
mm 




Class. 
Book 



COPYRIGHT DEPOSIT 



A TEXT-BOOK 



OF 



DENTAL PATHOLOGY 



AND 



THERAPEUTICS 



FOR STUDENTS AND PRACTITIONERS 



BASED UPON THE ORIGINAL OF 

HENRY H. BURCHARD, M.D., D.D.S. 

LATE SPECIAL LECTURER ON DENTAL PATHOLOGY AND THERAPEUTICS IN THE PHILADELPHIA 

DENTAL COLLEGE 



REWRITTEN BY 

OTTO E. INGLIS, D.D.S. 

PROFESSOR OF DENTAL PATHOLOGY AND THERAPEUTICS IN THE PHILADELPHIA 
DENTAL COLLEGE 

FIFTH EDITION, THOROUGHLY REVISED 
ILLUSTRATED WITH 708 ENGRAVINGS AND A COLORED PLATE 




LEA & FEBIGER 

PHILADELPHIA AND NEW YORK 
1915 



v <nv 



V 



Entered according to the Act of Congress, in the year 1915, by 

LEA & FEBIGER, 
in the Office of the Librarian of Congress. All rights reserved. 



JAN 13 1915 



'CI.A393255 

11 i' t 



-2L f?06> 

7^0 



THIS 
VOLUME 

IS RESPECTFULLY DEDICATED 
TO 

RUSSELL H. CONWELL, D.D., LL.D. 

IN RECOGNITION OF HIS UNSELFISH 

EFFORTS IN THE 

OPENING OF OPPORTUNITIES 

FOR EDUCATION. 



PREFACE TO FIFTH EDITION. 



This volume was originally designed as a text-book of the principles 
and practice of dental medicine for the use of students, and as a 
reference work on applied special pathology and therapeutics for 
the use of dentists. Accepting the dictum of the advanced teachers 
of the day, it was considered that an entirely rational system of 
dental medicine could have but one basis — namely, the same prin- 
ciples which underlie general medical and surgical practice. The 
book represents, therefore, an attempt at formulating, from data 
obtained from every available source, a system of dental pathology 
and therapeutics of which the several parts shall be in harmony with 
one another and also with the several collateral sciences involved. 
The impulse prompting the work was no desire to multiply books, 
but arose from a conviction expressed by many teachers, that such 
a volume was needed by students, practitioners, and teachers. 

In revising the work for this new edition, the Editor has endeavored 
to maintain the original idea of a text-book furnishing a description 
of each dental disease and its treatment in such manner that teachers 
may find it a useful adjunct in the presentation of dental pathology 
and therapeutics to their students. The development in this branch 
of dental science during the last few years has necessitated many 
changes in the text to reflect the present advanced position of the 
entire subject. Many new illustrations have been added to increase 
its value for didactic purposes. 

In place of the original section on Pharmacology, which was 
necessarily limited in scope, the various remedies and drugs men- 
tioned are fully indexed in order that their various uses as applied 
to the therapy of the pathological conditions discussed may be studied . 

The thanks of the Editor are due to those who have kindly loaned 
valuable illustrations. In no instance has a request been denied. 

The Editor also takes this opportunity to express his warm appre- 
ciation of the continued favor bestowed on this work by professors 
and teachers of the subject throughout this Continent and in Europe. 

0. E. Inglis. 

1524 Chestxut Street, 
Philadelphia, 1915. 



CONTENTS. 

SECTION I. 
GENERAL PATHOLOGY. 

CHAPTER I. 
General Principles 17 

CHAPTER II. 
Causes of Disease, General and Local 28 

CHAPTER III. 

Microorganisms as Exciting Causes of Disease 36 

CHAPTER IV. 

Disturbances of Nutrition 66 

CHAPTER V. 

Disturbances of the Vascular System 113 



SECTION II. 
EMBRYOLOGY, ANATOMY, AND HISTOLOGY. 

CHAPTER VI. 

The Development, Anatomy and Histology of the Jaws and Teeth 153 

CHAPTER VII. 
Dentition: Its Progress, Variations, and Attendant Disorders 194 

CHAPTER VIII. 
Malformations and Malpositions of the Teeth 239 



viii CONTENTS 

SECTION III. 
AFFECTIONS OF THE ENAMEL AND DENTIN. 

CHAPTER IX. 
Abrasion, Erosion, and Mechanical Injury 299 

CHAPTER X. 

Stains of the Enamel and Dentin 329 

CHAPTER XL 
Dental Caries: History; Exciting and Predisposing Causes . 337 

CHAPTER XII. 
Dental Caries: Pathology, Morbid Anatomy, and Clinical History 362 

CHAPTER XIII. 

Dental Caries: Diagnosis, Symptoms, and Prognosis 390 

CHAPTER XIV. 

Dental Caries: Therapeutics and Prophylaxis 416 



SECTION IV. 
DISEASES OF THE DENTAL PULP. 

CHAPTER XV. 
Constructive Diseases 447 

CHAPTER XVI. 

Destructive Diseases of the Dental Pulp 468 

CHAPTER XVII. 

Methods of Removal of the Dental Pulp and Root-canal Filling 515 

CHAPTER XVIII. 
Gangrene of the Pulp 562 



CONTENTS ix 

SECTION V. 
DISEASES OF THE PERICEMENTUM. 

CHAPTER XIX. 

Septic Apical Pericementitis (Acute) 585 

CHAPTER XX. 

Chronic Septic, Purulent, Apical Pericementitis (Chronic Apical 

Abscess) 609 

CHAPTER XXI. 
Xon-septic Pericementitis 644 



SECTION VI. 

PERICEMENTAL DISEASES BEGINNING AT THE 
GUM MARGIN. 

CHAPTER XXII. 
Gingivitis 673 

CHAPTER XXIII. 
Salivary and Serumal Calculus 692 

CHAPTER XXIV. 
Pyorrhea Alveolaris 713 

CHAPTER XXV. 

Pericemental Abscess 745 

CHAPTER XXVI. 
Reflex Neuroses 752 

CHAPTER XXVII. 
Infections of and from the Mouth, and Sterilization .... 766 



DENTAL PATHOLOGY AND THERAPEUTICS. 

SECTION I. 
GENERAL PATHOLOGY. 

CHAPTER I. 
GENERAL PRINCIPLES. 

General pathology {pathos, disease, and logos, a discourse) is that 
branch of science which treats of the modifications in function and 
changes in structure occurring in disease. It embraces all patho- 
logical processes occurring in the human body, and as many of these 
occur in and about the teeth, modified only by the peculiar anatomy 
of the parts, Dental Pathology may be said to be that branch of 
dental science which treats of modifications in function and changes 
in structure occurring in the diseases of the teeth and associate parts. 

This being true, it follows that the study of dental pathology must 
be preceded by a study of the general disease processes which affect 
the tissues of the body, and such of these as are applicable to the 
study are known as the General Principles. 

The word Therapeutics is derived from the Greek therapeuin, to 
take care of, meaning the measures adopted to remedy or remove 
the changes induced by pathological processes. 

The study of the pathology of a part begins with a study of its 
anatomy and histology, then naturally follows a study of its physi- 
ology and embryology. These form the basis from which degrees 
of abnormal function and altered structure may be judged by com- 
parison with similar processes occurring in other parts of the body. 

The body is composed of cells held together by intercellular sub- 
stance. These cells are the essential functionating parts of the 
organism; each cell is composed of a small mass of protoplasm 
containing in nearly all cases a nucleus, and has a form adapted to 
2 (17) 




18 GENERAL PRINCIPLES 

its environment and function. The exact chemical composition of 
protoplasm is unknown and efforts at analysis destroy its peculiar 
property as a substance exhibiting a sequence of phenomena called 
life. It is a viscid substance composed physically of a network, the 
spongioplasm, containing a slightly more fluid substance, the hyalo- 
plasm. 1 Chemically it is 70 per cent, water containing a collection 
of proteids, and differs as to these in the different classes of cells. 
Proteids are but imperfectly understood, but are known to consist 
essentially of carbon, hydrogen, oxygen, and nitrogen, combined 
with sulphur and other varying elements in enormous molecules 

approximately represented by the formula 
FlG - * C400H310O120N50S. 2 This formula represents 

merely the quantities of these elements, 
which are probably combined into various 
chemical compounds in the cell, including 
in some proteids one or more carbohydrate 
radicals, and each having its peculiar 
chemical affinity for food materials, and 
even irritating or poisonous materials, 
capacity for energy or function, and reduc- 
Changes of form in an tion to waste or use i ess ce n material. The 

ameba: PP, pseudopodia; . 

v, vesicle; N, nucleus. study oi the properties or cell protoplasm 

may be made by observing in situ the 
action of living cells under normal conditions, and when subjected 
to artificial stimuli, and by observing the action of free single cells, 
such as an ameba, under like conditions. 

If a drop of water be taken from the sides or bottom of an aqua- 
rium, placed on a slide and covered with a cover-glass, and then 
placed under a microscope with, first, a \" objective, there will be 
noted at some portion of the fluid a small transparent mass having 
the appearance of a colorless fragment of jelly; this is an ameba. 
The outline of the mass may have almost any form. At some por- 
tion there will be a defined and easily distinguished spot, the nucleus ; 
at another point a vesicle is seen; the body of the ameba appears to 
contain numbers of fine granules. The nucleus appears more mark- 
edly granular than the body of the ameba. If kept under obser- 
vation, the ameba will be seen to change its outlines; at one or more 
and it may be in several places, projections like blunt arms or feet 
are seen to be extending from the ameba (Fig. 1). On account of 
their appearance they are called by the physiologist pseudopodia, 
from pseudo, false, and pons, a foot — false feet. These changes of 

1 Kirke's Physiology. 2 Schofield, Elementary Physiology. 



PROPERTIES OF CELLS 



19 



form arc much varied (Fig. 2). The cell has, therefore, the property 
of altering its form — ?'. e., it has mobility and contractility; as by 
means of these motions it changes its location, it has the property 
of locomotion. 



Fig. 2 



%w p 




Ameboid movement of a white blood corpuscle of man; various phases of movement. 

(Klein.) 

When certain solid substances contained in the water come in 
contact with the ameba, the latter is seen to flow around and engulf 
them ; as is shown in Figs. 3 and 4, where the analogue of an ameba, 
a leukocyte, has taken in bacteria (phagocytosis). After a time the 
ingested body is found to have disappeared; it has been digested. 
Evidently the cell must produce a substance capable of dissolving 
some foreign substances — i. e., it has the function of secretion. This 
is due to a digestive enzyme analogous to trypsin, which has been 
experimentally isolated from the ameba. 1 More than this, the 



Fig. 3 



Fig. 4 




Leukocyte of a frog from the neighborhood 
of a piece of the lung of a mouse infected with 
anthrax, about forty-two hours after the piece 
of lung had been placed under the skin of the 
frog's back. The leukocyte is in the act of eat- 
ing up an anthrax bacillus. (Brunton, after 
Metchnikoff.) 




The same leukocyte a few 
minutes later, after it has com- 
pletely enveloped the bacillus. 
(Brunton, after Metchnikoff.) 



ameba does not take in substances indiscriminately; some it rejects. 
All cells change the chemical nature of the media in which they 
grow, both by exhausting the nutritive supply and ejecting their 
excreta. 

If the temperature of the slide be raised the movements of the cell 
become more rapid, and if raised to a temperature of 55° C. the 
cell contracts in a round lump; it responds to stimuli, and has 
therefore the property of irritability. 

If the stage be cooled, the movements of the protoplasm are 



1 Hiss and Zinsser, Text-book of Bacteriology. 



20 



GENERAL PRINCIPLES 



lessened, and when foreign substances come in contact with the 
cell it fails to encompass them — its irritability and contractility 
are lessened. 

It is noted that some simple cells are attracted and stimulated by 
light; others are repelled by it. 

If a mild induction (interrupted) current be passed through the 
water in which the ameba is, the movements of the cells are checked ; 
if a strong current be passed, the cell contracts sharply. If a gal- 
vanic (constant) current be passed, movement at first ceases, but 
pseudopodia are extruded toward the cathode and the cell crawls 
toward that pole. 1 

Fig. 5 




Forms assumed by a nucleus in dividing: a, resting nucleus; b, skein-form, open 
stage; c, wreath-form; d, aster, or star-form; e, equatorial stage of division; /, separa- 
tion more advanced; g and h, star and wreath forms of daughter nuclei. (Reduced 
from Flemming's drawings in the Arch. f. Mik. Anat.) 

The cell responds to mechanical stimuli, such as violent shaking, 
by contraction. 2 

If substances such as ether or chloroform are added to the fluid, 
the irritability of the cell is so lessened that it does not respond to 
stimuli. It is either chilled by evaporation or actually anesthetized. 

If the supply of oxygen be cut off, or if carbon dioxid be admitted 
to the fluid, movement ceases and the cell remains contracted. 

If the observations are continued, it will be noticed that changes 
occur in the nucleus of the cell. A series of alterations in its figure 
are noted, as shown in Fig. 5. Two nuclei are formed, and soon the 
body of the cell divides and two cells appear — the ameba has repro- 
duced itself. 

These observations serve to show that protoplasm as shown by 
the behavior of cells containing it has the properties of irritability, 
contractility, motion, selection, secretion, and excretion (i. e., met- 



1 O. Hertwig, The Cell. 



2 Ibid. 



PROPERTIES OE ('ELLS 21 

abolism or cell digestion) and reproduction, and that it responds to 
stimuli of physical and chemical nature, and that its functions may 
be altered by substances which are brought in contact with it. 
Upon these facts depends the practice of therapeutics, in which 
stimulation, sedation or alteration of nutritive function of the cells 
by means of the various drugs or remedies available is the aim of 
the therapeutist. 

A living organism, it will be seen, has a certain degree of action 
and function. The general average of its action and functions is 
spoken of as a condition of health. When from any cause the func- 
tions are raised or lowered or in any way chemically altered from 
the general average, a condition of disease exists. 

Stimulation. — Certain agencies applied to the cell increase its 
activity; this is called stimulation. The movements of the cell 
become more rapid, food particles are taken in more rapidly and 
disappear more quickly; irritability, contractility, and secretion are 
increased. The cell subdivides, or reproduces more quickly. In- 
crease the stimulation, and the vital activity becomes fretful; in 
some cases cell division is incomplete — the nucleus divides, but not 
the cell body. Increase the stimulation beyond this degree, and the 
wearied cell ceases its movements — refuses to respond; is paralyzed 
in the body by overwork. It has also been shown that the cell 
loses its essential substance in overwork and that sometimes the 
products of its activity are held about it, causing cessation of 
function. This may be restored, if not carried too far, by rest and 
nutrition or by rest and the removal of the waste product. 

Sedation. — If the conditions be reversed; if, instead of applying 
a stimulus to the cell, an opposite influence be introduced, the 
phenomena are reversed. 

If the temperature be reduced, the movements of the cell become 
sluggish ; the body changes its form more slowly and less extensively 
— i. e., contractility is lessened; particles taken into the cell remain 
apparently unchanged; irritability, secretion, and excretion are 
lessened; and, furthermore, reproduction does not occur nearly so 
rapidly — that is, the cell in contact with sedative influences has all 
of its activities lessened. This leads to paralysis and death of the 
cell — it is starved to death. 

Alteration. — It is to be understood that the cell is a microscopic 
laboratory conducting complex chemical processes which may be 
altered by an infinite number of influences of subtle nature. This 
modification may possibly occur in a manner not referable to simple 
stimulation or sedation, as, for example, by retention of waste, or 
depositon of matter extraneous to the cell. Such changes may 



22 GENERAL PRINCIPLES 

fittingly be spoken of as alterations, especially in view of the behavior 
of cells when subjected to the influence of that class of drugs known 
as alteratives or such influences as sunlight or the psychological 
remedies. While such alterations also probably occur as the result 
of stimulation and sedation, the fact that the beneficial action of 
certain classes of therapy is not understood warrants this third 
classification even if for explanatory reasons only. The term mal- 
nutrition is synonymous with alteration as here described. 

Every cell has a range of resistance to these influences which tend 
to destroy it, which is fitly termed the resistance of vitality. Disease 
itself is some alteration in the cell chemistry controlling any one or 
more of these several cell properties, of irritability, contractility, 
growth, secretion, maintenance, or reproduction. If any one of 
these properties is not exhibited, it is said that the cell is diseased. 

The cell lives its cycle and reproduces, and the parent is no more, 
the life being, continued in the offspring. 

The life and properties of this small mass of protoplasm represent 
in miniature the primitive functions and life of the highest animals. 

The contractility is represented in the motive apparatus of the 
higher animals. 

The reception, engulfing, and dissolving, or casting out, of bodies 
with which the ameba is brought in contact correspond in the higher 
animals to the digestive apparatus and process and the excretory 
function. 

The highly evolved irritability is represented in the nervous 
system of the higher animals. 

The movements occurring in and about the vacuole are the pro- 
genitors of the circulatory apparatus and all of its adjunct organs. 

If the irritability of a simple cell be increased or diminished, it 
corresponds to a disease of the nervous system, and so with the 
other functions. 

In the human body certain collections of cells are found in which 
one function is active, the others in abeyance; thus, large colonies 
of cells exist in which contractility is the dominant property noted; 
these are muscle cells. Others have but the property of irritability; 
these are nerve cells. Still others develop peculiar chemical func- 
tions, and become glandular or secretory cells. Such collections of 
cells are known as tissues. These special cell colonies or tissues are 
built together into defined masses for the performance of their 
specialized functions. In the development of these masses, means 
of holding and maintaining the cells in definite mass forms and 
provisions for their food supply and waste-removing apparatus 
are provided in what are called the connective tissues, binding the 



NUTRITION 23 

colls iii definite forms and transmitting their vascular supply (food- 
and waste-carrier). When thus hound together the tissues are said 
to form organs. 

While all tissues are capable of analysis into cells and intercellular 
substance, a more practical view may resolve the tissues into (1) func- 
tional cells; (2) a supporting intercellular substance; (3) intercellular 
spaces in which flows the lymph derived from the blood; (4) the 
channels of circulation and conductors of nervous impulses — i. e., 
arteries, capillaries, veins, lymphatics, and nerves. The arteries 
bring to the tissues the blood freighted with oxygen and nutrient 
material. As it passes through the capillaries a portion of the blood 
plasma, under arterial pressure and osmotic force, passes into the 
intercellular spaces into contact with the cells. This exuded fluid 
is now called lymph. 

Stated in general terms, the food materials contained in arterial 
blood and furnished to the tissues by way of the lymph are water, 
some proteid, and the constituent to make proteid, amino-acids and 
polypeptids, 1 glucose and fats or their elements, inorganic salts, 
and oxygen. From this store the cells take what they require, and 
within themselves they elaborate chemically substances essential to 
their growth and maintenance as masses of functionating protoplasm 
(anabolism). As the protoplasm is of more complex composition 
than the majority of food elements, they are said to form from simple 
compounds substances of a higher degree of complexity. Having 
performed its functions, or in the act of such performance, this 
protoplasm is chemically altered into waste products of less complex 
chemical composition (catabolism) and such " products of catabo- 
lism" are thrown out from the cell into the lymph in the inter- 
cellular (lymph) spaces. This process may be spoken of as cell 
elimination and the substances themselves as cell ejecta. The total 
process is termed metabolism. 

While the exact nature of the chemical change occurring in cells is 
not known, the present thought is that much of the process of cell 
metabolism is conducted wathin the cell through the action of one 
or more enzymes which have the power of catalytically effecting 
prompt and smooth chemical changes at low temperature, which can 
at times be produced in the laboratory only by complicated experi- 
ments not at all comparable with the action of cells. 

Various organs of the body evidently prepare the food material 
absorbed by the intestines for the use of the cells — for example, gly- 
cogen is formed from the absorbed glucose by the ferment of liver 

1 Howell, Text-book of Physiology, 1911, p. 877. 



24 GENERAL PRINCIPLES 

cells, and when needed again is transformed into glucose. As a 
proteid example the fibrinogen of the blood is supposed to be pro- 
duced in the liver. 1 The proteid as built into complete form in the 
body juice and tissues is very complex and may contain all or a 
portion of fourteen or more monoamino-acids or four or more 
diamino-basic bodies, which shows the tremendous problem of the 
chemical study of metabolism, which is as yet imperfect. 2 

Ehrlich's side-chain theory for immunity (which see) presupposes 
the presence of atom groups of protoplasm surrounding a complex 
group of atom groups, the nucleus, each atom group having affinity 
for a particular form of substance presented to it. These he terms 
receptors, and each is supposed to possess a combining or prehending 
group of atoms called an haptophorous group and a ferment group 
capable of altering the chemistry of the food element to suit its needs 
or that of the cell as a whole; this latter group is termed a zymoph- 
orous group. This obviously is merely stating in a scientific manner 
that the cell receives and digests food materials. The carbohydrates 
and fats are in the main the producers of energy, and are, lastly, 
resolved into glucose and fat or their elements for the consumption 
of the cells, and by them appropriated into their protoplasm, whence, 
by catabolic changes, they are started upon their retrogressive 
course to the final products CO2 and water. The proteids are mainly 
useful for the building of the cell protoplasm and its maintenance, 
and when catabolized end in products which in other organs are 
transformed into urea and uric acid. 

There is evidence that changes occur in the cell waste either in the 
blood or in various organs of the body. While, then, the bodily ejecta 
contain substances fairly constant in composition, they are held to 
represent elaborations of cell waste rather than actual cell ejecta. 
For example, urea is pretty certainly derived from muscular tissue, 
yet is nearly absent in muscle and is supposed to be due to the dehy- 
dration of ammonium carbonate in the liver. 3 Lactic acid and ammo- 
nium carbonate have been experimentally shown to be probably com- 
bined into uric acid in the liver. The cell waste is carried by the 
lymph into the lymphatics connecting with the intercellular spaces. 
Thence it is delivered by way of the venous system to the circulation, 
for further elaboration and elimination from the body. Any inter- 
ference with such elaboration or elimination must of necessity result 
in a retention of waste products within the system, probably leading 
to irritation and disturbance of metabolism in all cells. 

Cell metabolism is a chemical change and is therefore accompanied 

1 Howell, Text-book of Physiology, 1911, p. 444. 2 Ibid., p. 986. 

3 Kirke's Physiology. 



NUTRITION 25 

by heat production. Energy is stored up in the cell as latent force 
existing in actual cell substance and is capable of liberation under 
stimulus, which force is expressed in various forms of functional 
activity — /'. e. } contractility in muscular tissue, irritability and men- 
tality in nervous tissue, secretion in the various secretory glands, 
eliminative selection in the various excretory organs, etc. Experi- 
mental evidence has shown that after energy has been liberated to 
the point of fatigue, there is an actual loss of substance by the cells, 
in consequence of which they become smaller and of different his- 
tological appearance. It is evident, therefore, that any condition 
which will produce an expenditure of energy without a compensating 
restoration of cell material must result in a malnutritional process. 
Oils after a period of activity undergo degenerative processes, 
and are removed or are reproduced bv the process of mitosis 
(Fig. 5). 

The life conditions of cells are necessarily those under wdiich they 
best perform these functions without exhaustion, and are the fol- 
lowing: (1) a proper food supply, including water and oxygen; (2) 
a proper removal of waste products; (3) proper physical conditions, 
including a proper temperature; (4) possibly a proper innervation. 1 
Any interference with these conditions, which may be termed the 
normal physiological conditions, results in a morbid process of 
physiology or pathology in its limited sense. With such interfer- 
ence disease may be said to begin. The definition of disease as 
an alteration of nutrition is therefore appropriate. For this reason 
the proximate exciting causes of disease are classed as (1) abnormal 
food supply; (2) abnormal waste removal; (3) abnormal physical 
conditions; (4) abnormal nerve supply. 

The morbid physiology results in morbid products or in retained 
normal products and an altered cell function. When pronounced 
this is spoken of as Functional Disease, although it may be said to 
be in existence even if discomfort be not produced. Sooner or later 
an abnormal change in the histological characteristics of the cells 
or intercellular substance may occur, which has been referred to as 
Morbid Histology or Pathological Histology. As definite micro- 
scopic and often macroscopic appearances are associated with certain 
diseased conditions, these are referred to as the Morbid Anatomy of a 
disease or Pathological Anatomy. The phemonena associated with a 
disease are called its Semeiology (semeion, a mark or sign) or Symp- 

1 While this conception is practical, experiments at the Rockefeller Institute have 
shown that, kept in a proper aseptic nutritive fluid at a low temperature various 
organs and tissues may be preserved for a considerable time and even shipped, thus 
being available for surgery. This shows that cells possess a life only dependent upon 
the body as a whole for their source of nutritive supply. 



26 GENERAL PRINCIPLES 

tomatology, and are either described by the patient as sensations or 
pains of varied character or situation (Subjective Symptoms), or may 
be noted by normal or aided vision, by physical examination, 
chemical analysis or positive reactions to certain biological tests 
(as in the Wassermann reaction for syphilis) (Objective Symptoms). 
That which excites a disease or promotes the action of the excitation 
is called a Disease Cause. The study of disease causes is Etiology 
(aetios, a cause, and logos). It is noted that diseases having a fairly 
defined pathology and morbid anatomy have from their beginning 
to ending tolerably constant phenomena; they have each a natural 
history; this is called the Clinical History of a disease. 

The study of the origin and development of a disease together is 
known as its Pathogenesis (pathos, disease; gennao, I produce). 
Through the study of the characteristic symptoms of diseases, as 
well as those common to several diseases, a particular disease may be 
distinguished. This is called Diagnosis (dia, through; gignosko, I 
know) — Direct Diagnosis when there is no question as to the symp- 
toms, Differential Diagnosis when several diseases are possible and 
the characteristics of one are considered as more pronounced. Under 
certain circumstances a disease may be inferred to be present by 
excluding all other possible conditions (Diagnosis by Exclusion). A 
fourth method of diagnosis is by the therapeutic test (see below) . In 
the course of a disease experience has shown that certain signs and 
symptoms are apt to be followed by good or ill results, as the case 
may be. By these signs and symptoms it may be foretold with some 
degree of assurance what will be the probable outcome of the disease. 
The inference based upon these symptoms is known as the Prognosis 
(pro, before, and gignosko, I know). The care of or treatment of a 
disease is its Therapeutics. This involves a knowledge of remedies 
applicable, known as the Materia Medica. When applied upon the 
basis of a scientific study of the pathogenesis, clinical history, and 
prognosis of disease and a parallel knowledge of the physiological 
action of drugs and of other remedies, the treatment is known as 
Rational Therapeutics. When the treatment is based upon the 
known good effects of a remedy in a certain disease, and not upon 
its physiological action, it is known as Empirical Therapeutics. 
Diagnosis may not always be clear, but upon a basis of previous 
experience of association of symptoms a given therapeutics may 
be applied with more or less rationality. Whether good results 
follow or not the method is known as "the therapeutic test." 

The pathogenesis of a disease being known, intelligent efforts may 
be exerted for its prevention. The causes may be removed or neutral- 
ized before they have an opportunity to act; this is Prophylaxis. 



NUTRITIOX 27 

The science of prevention of disease upon the broad basis of a 
knowledge of disease causes and observance of laws of health is 
Hygiene. 

It will be seen that a knowledge of special pathology can only be 
obtained from (1) a knowledge of pathology in general or at least of 
those principles of general pathology which underlie all disease pro- 
cesses; (2) a knowledge of the local anatomy and histology; (3) a 
knowledge of local embryology and physiology ; (4) a study of local 
pathology and morbid anatomy. To this must be added a study of 
materia medica and special therapeutics. 



CHAPTER II. 
CAUSES OF DISEASE, GENERAL AND LOCAL. 

A disease cause may be defined as any influence of whatsoever 
nature which is capable of disturbing the nutritive balance of any 
portion of the body. The branch of study which deals with the causes 
of disease is called Etiology. 

The causes of disease are classed as Exciting (or Determining) 
and Predisposing. These are each divisible into Extrinsic, originating 
from without, and Intrinsic, originating within the body. 

EXCITING CAUSES OF DISEASE. 

These are influences, either extrinsic or intrinsic, which are com- 
petent to suddenly or gradually interfere with the nutrition of the 
cells of a part or with the general nutrition of cells. These influ- 
ences are very numerous, but may be grouped according to their 
action under a few convenient headings: (1) Abnormal Food Supply. 
(2) Abnormal Waste Removal. (3) Abnormal Physical Conditions. 
(4) Abnormal Nerve Supply. 

These are termed the Proximate Exciting Causes, as their effects 
are immediately exerted upon the cells. Other causes may be back 
of these and are spoken of as Primary (or Contributory) Causes — 
e. g., tuberculosis of the lung (primary) may cause insufficient 
oxygenation of the blood which constitutes an abnormal food supply 
(proximate). 

Abnormal Food Supply. — By abnormal food supply is meant an 
altered quantity or quality of nutritive elements delivered to the 
cells either of a part or of the entire body. The primary causes of 
this may exist as disturbances or faults in any of the food-elaborating 
organs, the lungs, the eliminating organs, or the oxygen carriers of 
the blood may exist in lessened numbers. In the first case the quality 
or quantity of nutritive material is impaired, in the second and fourth 
cases oxygenation is insufficient, and in the third case materials in- 
jurious to cells are retained in the body and are again presented as 
food to the cells, acting as poisons. Poisonous or even non-poisonous 
drugs, and the products of bacterial action, whether absorbed from 
the intestines or from foci of infection, have all more or less delete- 
rs) 



EXCITING CAUSES OF DISEASE 29 

rious action upon cell protoplasm, violent if entering the blood in 
large quantity, chronic if entering continuously in small quantities. 

Faults in the circulatory apparatus, interfering with the circulation 
generally, cause an interference with general nutrition, while local 
disturbances of the circulation from any cause disturb the relations 
of the blood supply to the nutrition of a part. Thus the fresh blood 
supply (food supply) to a particular location may be excessive, as 
in arterial hyperemia, or deficient, as in venous hyperemia and 
inflammation. 

Abnormal Waste Removal. — Abnormal waste removal is ordinarily 
included under the heading of abnormal food supply, and it is 
evident that retention of waste in the blood causes the presentation 
to cells of an abnormal food or poison. In local conditions, such as 
venous hyperemia and inflammation, the stasis causing waste reten- 
tion prevents the access of a fresh food supply as well. In kidney 
disease the substances ordinarily physiologically eliminated by the 
kidneys are retained in the blood and act as poisons to cell proto- 
plasm generally. Insufficient circulation of lymph about cells 
means a relative retention of waste products about the cells with 
its effects upon them. 

Abnormal Physical Conditions. — This class of disease causes 
includes all injuries due to any of the physical or chemical forces: 
Traumatic injuries, such as cuts, bruises, surgical openings, etc. 
Mechanical causes, such as compressions, obstructions to ducts or 
the natural outlets of the body, faults in the circulatory mechanism, 
stoppages in the arteries or veins. Chemical causes, such as the 
action of abnormal temperatures, burns, freezing, or irritations of 
various sorts, such as those due to mustard, arsenic, acids, or caustics, 
and the local effects of microorganisms may all be classified under 
this heading. The disturbance is due to either a direct destruction 
of the life of the cells or an interference with the circulation in a part. 

Abnormal Nerve Supply. — It is known that division of, injury to, 
or disease of certain nerves causes trophic or nutritional changes in 
the part to which they are supplied. Whether the nutrition of the 
parts is controlled by special trophic nerve fibers has not been 
demonstrated. Halliburton, 1 in support of the trophic influence 
of nerves, instances that when the fifth nerve (sensory) is divided 
beyond the Gasserian ganglion, ulceration of the cornea results; 
while if the seventh nerve (motor) be divided or paralyzed, the eye- 
ball *is equally exposed to irritants, yet does not ulcerate. He also 
instances that division of the vagi produces fatty degeneration of 
the heart. 

1 Kirk's Physiology. 



30 CAUSES OF DISEASE, GENERAL AND LOCAL 

While admitting the lack of anatomical proof, he regards the 
trophic influence of nerves upon parts to be unexplainable upon 
the ground taken by others, that all apparently trophic changes 
are due to disturbances of the vasomotor nerves controlling the 
caliber of vessels. According to these other observers degrees of 
dilatation are produced which modify the amount of blood delivered 
to a part and thus modify its nutrition. 

Effects are produced upon nutrition by causes which can act 
only through the nervous system — e. g., the effect of anxiety upon 
appetite and digestion. The interdependence of these classes of 
causes is almost self-evident; for example, constant suppuration at 
a focus of infection (abnormal physical condition) may induce a 
toxemia (abnormal food supply) which may be responsible for kidney 
or other disease (abnormal physical condition), resulting in the 
retention of waste products in the blood (abnormal waste removal 
or food supply), which has a vicious result upon all metabolism, 
including that of the nervous system, inducing in turn an abnormal 
nerve supply and lessening resistance even in the tissues about the 
original focus of infection. Such a train of events is known as the 
establishment of a vicious cycle and is interesting as related to the 
lessened resistance produced in the gingival tissues in pyorrhea 
alveolaris. 

PREDISPOSING CAUSES OF DISEASE. 

A predisposing cause of disease is one which influences the cells 
or juices of the body or part in such a manner as to lessen the 
resistance to the action of the exciting causes of disease. 

It must be considered that a predisposition or lessened resistance 
is in itself a condition of disease, not recognizable, perhaps, yet a 
departure from the standard of the best health of an individual or 
part. For the most part predisposition is regarded in its relation 
to the extrinsic causes of disease, such as bacterial influences. In 
such a condition the individual is said to be susceptible. (Suscep- 
tibility.) Predisposition is either general or local. 

General Predisposition. — This is either (1) a natural or inherent 
lack of resistance to infectious or non-infectious diseases, or (2) an 
acquired lack of resistance to infectious or non-infectious diseases. 
The human race in general is naturally predisposed to many infec- 
tious diseases, such as tuberculosis, cholera, malaria, measles, small- 
pox, typhoid fever, scarlet fever, and syphilis. 1 When a person is 
exposed to the disease and contracts it, he is said to be predisposed 

1 Ziegler, General Pathology. 



PREDISPOSING CAUSES OF DISEASE 31 

or susceptible to it. If he does not contract it, his system is immune 
either temporarily or permanently. (See Immunity.) There being 
several forms of immunity, the lack of any natural form may be 
considered as a predisposition. This immunity is ordinarily opera- 
tive when the individual is in the best state of health, and when a 
departure from this standard is brought about by any cause, exciting 
infective causes may then act. This is acquired predisposition. 
Some individuals have a natural or congenital lessened resistance 
to external influences of a non-infectious character, such as heat or 
cold, mental effort, or nervous irritations of a degree ordinarily 
borne by the great majority of individuals.- This may also be ac- 
quired, as, for example, by extreme subjection to the above or other 
enervating causes. An inherited predisposition to such diseases as 
insanity, cancer, or gout may exist. 

Some persons cannot bear certain kinds of food without illness, or 
react strongly to small doses of drugs, or are not affected by large 
doses. This is called an idiosyncrasy, and may be either congenital 
or acquired. 

The predisposing causes capable of producing a lessened resist- 
ance may be grouped under a few headings. 

Sex as an Intrinsic Predisposing Cause. — In this connection the 
influence of sex upon predisposition to disease must be considered. 
While the general resistive power of the bodies of both sexes may 
be regarded as practically equal under similar conditions, yet the 
anatomical structures and physiology of each sex have an influence 
upon predisposition to certain diseases. Aside from the diseases 
peculiar to sex, on account of their peculiar organs, each sex exhibits 
predispositions to diseases which the other sex escapes; for many 
of these the habits of life furnish an explanation, for others an ex- 
planation is not available. For example, males are much more 
subject to hemophilia than females. 

Age. — During the first two years after birth the nervous system 
and the appendages of the alimentary canal are developing, and 
improper feeding, difficult teething, or other influences readily act 
as exciting causes of alimentary or nervous disturbances. 

Later, children are subject to acute infectious diseases, especially 
tuberculosis, diphtheria, and the eruptive fevers. At adolescence 
other predispositions occur, notably chlorosis in young girls. Later 
come the diseases of early maturity, such as typhoid fever, pulmo- 
nary tuberculosis, and to a degree dental caries. 

In old age or middle life occur arterial and other degenerations 
and diseases consequent upon them or upon overstimulation of 
organs or tissues. 



32 CAUSES OF DISEASE, GENERAL AND LOCAL 

Temperament. — Temperament is the peculiar congenital consti- 
tution of an individual imparting certain' physical characteristics 
and certain natural tendencies. There are four basal temperaments: 

The sanguine is that in which individuals are decidedly inclined 
to the blonde type, with evidence of an abundance of the nutritive 
fluid, the blood — i. e., the vascular system is said to dominate the 
other functions of the body. Such are predisposed to acute pul- 
monary and cardiac diseases and inflammatory disturbances of 
serious import. The mental characteristics of this temperament 
are hopefulness, cheerfulness, and solidity but floridity of mental 
endowments. The recuperative power is good. 

The bilious temperament is characterized by a decided inclination 
to the brunette type, with evidence of a domination of other func- 
tions by the liver. There is a tendency to hepatic and digestive 
derangements and despondency; at the same time there is pos- 
sessed great physical and mental strength, together with a reliable 
recuperative power. 

The nervous temperament is indicated by the smallness and 
delicacy of frame and the quickness of motion and perception, 
evidencing a domination by the nervous system, to diseases of 
which such temperament predisposes. In such individuals disease 
is usually of rapid course, and recuperation is rather more rapid 
than reliable. 

The lymphatic temperament is indicated by bulk, pallor, and flac- 
cidity of tissue, a colorlessness of temperament, indicating an inherent 
feebleness. There is a tendency to serious chronic conditions. This 
temperament is accompanied by poor recuperative force. 

There are no individuals of pure basal temperament, so that the 
nearest approach is a dual or binary temperament, such as the 
biliosanguine, in which the characteristics of the sanguine predomi- 
nate, strongly modified by those of the bilious temperament. In 
like manner the sanguonervous, nervolymphatic, and other classes, 
twelve in number, are recognized as having typical representatives 
in each community. A third or ternary classification is possible — 
e. g., sanguonervobilious. It will be seen that temperament has a 
distinct relation to the vital resistance normally implanted in an 
individual, and therefore may to a certain extent be counted upon 
in a prognosis. Temperament is a predisposing cause probably only 
in so far as it introduces a natural general lack of resistance to disease, 
or irresistibly drives an individual into certain habits of life which 
may become the cause of a lessened resistance. The writer is aware 
that question has been raised as to even the existence of such a thing 
as temperament. It is true that the Chinese, Negro, Arab, etc., 



PREDISPOSING CAUSES OF DISEASE 33 

have not been included in the above classifications. As applied 
to the Caucasian race, however, what is said above is intended to 
convey the meaning that there is a combination of mental and 
physical characteristics which, apart from education or environment, 
influence the tendencies of individuals. 

Heredity. Certain diseases exhibit a predisposition to descend 
from parent to child direct, or from grandparent through the un- 
affected son or daughter to a grandchild (in the latter case it is called 
atavistic hereditary transmission, also remote heredity). 

The mode of transmission is in all probability the inheritance of 
a type of tissue, a tissue anatomy and physiology which permit the 
more ready action of the exciting causes of the disease. This ten- 
dency is called a diathesis — e. g., hemorrhagic diathesis (hemophilia), 
gouty diathesis, or tuberculous diathesis. Diathesis may also be 
acquired. The influence of race may also be considered as coming 
under this heading. (See Immunity.) 

Existing Disease. — The presence of one disease may w r eaken the 
resistance of a part or the organism so that another disease may 
the more readily become implanted — e. g., measles followed by 
pneumonia; diabetes accompanied by pyorrhea alveolaris. In 
diabetes the opsonic index may be reduced one-half. McFarland 
states that when glucose is present in excess in the blood (glycosuria 
as in diabetes), susceptibility to infection is increased. 

Previous Disease. — At a period subsequent to disease the same 
disease may recur or another disease may be implanted — e. g., 
pneumonia predisposes a lung to a recurrence of pneumonia, or 
tuberculosis may readily follow. Previous disease may confer 
immunity to the same disease, as, for example, in smallpox or 
measles. 

Extrinsic Predisposing Causes of Disease.— Under this head are 
included all those conditions of external origin which lessen the 
resistance of an individual to the action of exciting causes. Excessive 
heat is weakening; cold and dampness, by chilling the surface of 
the body, cause hyperemia of internal parts and thus predispose to 
such diseases as pneumonia, rheumatism, etc. Fatigue, unhealthy, 
cramping, or sedentary occupations, continued loss of sleep from 
any cause, evil habits, continued hunger, etc., are other examples of 
debilitating influences wmich may be partly intrinsic. 

Local Predisposition. — Alterations in the normal physiology of 
a pact are apt to occur through certain actions upon it, thus bringing 
it into a condition of lessened resistance, permitting the action of 
entirely different exciting causes. Apart from this fact, a part may 
be predisposed, by nature apparently, to permit the growth of 
3 



34 CAUSES OF DISEASE, GENERAL AND LOCAL 

bacteria which do not grow well in other tissues. Local depression 
of tissue vitality predisposes to the growth of organisms in the tissues. 
Thus slight injury producing either arterial or venous hyperemia or 
ischemia may permit bacteria to produce even grave consequences. 
More severe injury also may predispose, but the contrary effect has 
also been observed — i. e., that severe injury excites a phagocytic 
reaction and copious exudation of lymph (a later stage of inflamma- 
tion) which antagonizes the bacteria. (See Inflammation.) 

The structure of a part has also been shown to have an effect upon 
the life of microorganisms gaining access to its tissues. The tissues 
about the mouth are normally notoriously resistant to infections, 
but at times are exceedingly susceptible, as in pyorrhea alveolaris. 
Ordinarily surgical operations about the mouth were successful in 
pre-aseptic times, w T hile abdominal or gynecological operations were 
attended by an enormous percentage of. death from infection. 
General depression of vitality also necessarily affects the resistive 
force of all local tissues. Thus extensive suppuration is more liable 
to occur in those rendered feeble and anemic by any cause. 

IMMUNITY. 

Immunity is the opposite of predisposition, and, like it, can be 
either natural or acquired. It signifies an insusceptibility to a disease. 
Natural immunity to a particular infectious disease can only be 
determined by repeated exposures, and may then fail at last owing 
to some systemic change. 1 Immunity may be exhibited toward 
only one disease. In some persons disease appears to be influenced 
by sex, as, for example, males have a general immunity from goitre, 
females from Addison's disease. Immunity is influenced by age in 
certain diseases; for example, the diseases of childhood are rare in 
the elderly; they do occur, however. The degenerative diseases of 
old age are almost unknown in childhood. Race has its influence; 
the negro is almost immune to malaria and yellow r fever, but particu- 
larly susceptible to smallpox and tuberculosis. Some have explained 
this on the ground that in localities in which malaria and yellow 
fever are endemic the disease has been acquired in early life and 
that an apparent natural immunity is really an acquired immunity. 
Inheritance of amboceptors from immune ancestors has been offered 
as an explanation. The natural immunity may be more apparent 
than real, owing to failure of the bacteria to find a local condition 
favorable to development and to enter the blood. If special care 

1 Green, Pathology and Morbid Anatomy. 



IMMUNITY 35 

in experiment be taken to introduce the bacteria, and failure of 
inoculation result, the natural immunity is absolute. Example: 
Rats to diphtheria, or negroes to yellow fever. 

A striking example of lost immunity occurred in the case of a 
friend, who, in early and middle life, could handle poison ivy with 
impunity. On approaching seventy years of age, and while in a 
condition of general debility, he was affected from head to foot with 
the peculiar dermatitis as the result of pulling up a plant. 

The further discussion of immunity as related to bacterial infection 
should properly be discussed after the consideration of bacterial 
causes, and will be found at the end of Chapter III. 



CHAPTER III. 



MICROORGANISMS AS EXCITING CAUSES OF DISEASE. 



The infectious and contagious diseases have for the most part 
been shown to be caused by low forms of vegetable organisms known 
collectively as fungi, while in a few diseases minute animal organisms 
(protozoa) are the causes. 

The following table shows the position of the vegetable organisms 
in the scale of vegetable life and gives the lowest forms of animal 
life: 



Vegetable 
kingdom 



Animal 
kingdom 



Phanerogams: plants reproducing by flowers and seeds. 



Cryptogams, 
reproducing 
by spore 
formation 
or division. 



Lowest forms 



Higher forms. 



Lichens. 
► Alga?. 

Fungi. 



Leafy cryptogams 
Thallophytes, 
having no dis- 
tinction be- 
tween the 
leaf and stem 



Protozoa: single cells 
without circulatory or 
nervous systems. 



Basidiomycetes. 
My corny cetes. 
Phycomycetes. 
Saccharomycetes. 

Schizomycetes. 



Favus fungi. 
Common molds. 
Mucor molds. 
Yeasts or blasto- 

mycetes. 
Bacteria. 



Sarcodinea. 
Flagellata. 
Sporozoa. 
Infusoria. 



Mycetozoa, fungi not certainly defined as animal or vegetable 

forms. 1 
Certain insect and worm forms are pathogenic. 



Fig. 6 




Trichophyton tonsurans 
("barbers' itch"). (Myco- 
mycetes.) Diagrammatic. 
(Lehmann.) 



Of the protozoa four classes are known, 
though but few species are pathogenic; these 
classes are (1) the sarcodinea (ameboid), 
which includes the Ameba coli of dysentery 
(Fig. 10); (2) the flagellata, non-ameboid 
but motile by means of flagella; (3) the 
sporozoa living within the bodies of other 
animals, a class which includes the hemo- 
sporidia, ameboid motile parasites living 
in the blood, and of which the malarial 
germs, Plasmodium malarise (quartan fever, 
seventy-two-hour cycle), the Plasmodium 
praecox (estivo-autumnal fever, twenty- 



1 The terms mycetozoa and protozoa seem to be practically synonymous to path- 
ologists, who use the term protozoa in the sense of mycetozoa as above defined. 
(36) 



MICROORGANISMS AS EXCITING CAUSES OF DISEASE 37 

four or forty-eight-hour cycle, Fig. 11), the Cytorrhyctes variolar 
sen vaccina (the probable cause for smallpox and chickenpox) are 
examples; (4) the infusoria. 



Fig. 7 



Fig. 8 




Penicillium with spores. (Myeomyeetes, 
non-pathogenic.) (Lehmann.) 




a, saccharcmyces; b, cell with four 
spores. (Lehmann.) 



Fig. 9 



Fig. 10 




1, ameba from dysenteric 
stool, with vacuoles and in- 
closed red cells; 2, ameba 
from straw infusion ; 3, the 
Saccharomyces (oidium) albicans. (After Grawitz, same encysted. X 600. 
in Lehmann.) (Kunster.) 



38 MICROORGANISMS AS EXCITING CAUSES OF DISEASE 

Sonic of the protozoa act by entrance to the intestinal tract as 
Ameba coli of dysentery; some by direct contact of the healthy 

Fig. 11 




Plasmodium prsecox (forty-eight hours). Cycles of estivo-autumnal parasite 1, 
very young form; 2, infection of one cell with seven young parasites (drawn from a 
marrow smear); 3, triple infection, two parasites joined by single chromatin mass; 
4, double infection, peculiar rings with two chromatin grains at opposite poles; 5, 
double infection, small ring adherent to cell; 6, 7, signet ring forms, subdivision of 
chromatin; 8, 9, later ring forms, with subdivided chromatin and few pigment grains; 
10 to 12, full-grown forms, with finely subdivided chromatin and gradual concentra- 
tion of pigment; 13, 14, stages of presegmenting forms, with concentrated eccentric 
pigment; 15, double infection, with separate presegmenting bodies; 16, estivo- 
autumnal rosette; 17, 18, young crescent and ovoid; 19, "pulsating" crescent; 
20 to 22, various forms of crescents; 23, two bows about single crescent; 24, fully 
developed crescent, two masses of chromatin, achromatic substance, double wreaths 
of pigment; 25, diagrammatic flagellating body; 26, extracellular sterile body. 
(Schmaus and Ewing.) 



with the diseased surface or the infected object, as Treponema 
pallidum of syphilis (not yet positively classed with the protozoa) 
or Trepanosoma equiperdum of equine syphilis (Dourine). Some 



MICROORGANISMS AS EXCITING CAUSES OF DISEASE 39 

act only through an intermediary host as in the case of the Plas- 
modia of malaria through the anopheles mosquito. For a more 
extensive description of the action of protozoa, see works on general 

pathology. 

Fig. 12 






a b c 

a, spiral forms with a flagellum at only one end; b, bacillus of typhoid fever with 
flagella given off from all sides; c, large spirals from stagnant water with wisps of 
flagella at their ends (Spirillum undula). (Abbott.) 

The vegetable fungi are divided into (1) Basidiomycetes, which 
form spores borne upon basidia. The Achorion schonleinii, cause 
of tinea favosa or favus, a disease of the hair, usually of the head, 
is an example. (2) Mycomycetes (common molds) many-celled, 
characterized by mycelium. Form sporangia, conidia, and asci. 
Example: Oidium albicans, cause of thrush and aphthous ulcer, 
frequently in the mouth. Trichophyton tonsurans, cause of barbers' 
itch. (3) Phycomycetes (mucor molds). Resemble algse, but 
destitute of chlorophyl; occasionally pathogenic in man. (4) Sach- 
aromycetes (Blastomycetes), yeasts. Useful in vinous and bread 
fermentation; occasionally causes a vegetative dermatitis called 
cutaneous blastomycosis. 1 (5) Schizomycetes, or bacteria. Being 
without chlorophyl (the green coloring matter of plants which 
synthesizes C0 2 and water into starch), the fungi are unable to utilize 
the simple compounds, such as carbon dioxid and ammonia, as foods, 
and are therefore compelled to break down the complex organic 
compounds, for which purpose they are competent by reason of their 
enzymes. All classes of fungi have representatives which produce 
disease in the human body, but the schizomycetes furnish by far 
the greater number of infectious disease causes. 

Chemically, bacteria are about 85 per cent, water, together with 
albumin, called mycoprotein, ferments, soluble extractives, salts, 
sometimes nuclein bases, coloring matters, organic acids, sulphur, 
starch, and cellulose. 

The schizomycetes (Greek schizo, to split, and mukes, a fungus) 
are minute single-celled plants without nuclei, but possessed of a 

1 See Hyde and Montgomery, Diseases of the Skin. 



40 MICROORGANISMS AS EXCITING CAUSES OF DISEASE 

cell wall and cell protoplasm (mycoprotein). They have a size of 
about 1 micron (1m=2T1to"o inch) or less in their smallest diameter. 
Some of them possess rlagella, hair-like processes, often very numer- 
ous, arising from the protoplasm rather than the wall, with which 

Fig. 13 




Typhoid bacilli stained by Van Ermengem's method to show flagella. 

they lash the fluid surrounding them, and by which means they 
effect locomotion (Fig. 12). Other bacteria again are non-motile. 
Entering the organic compounds, carbohydrates, hydrocarbons, and 
nitrogenus (albuminous) substances, they ferment or decompose 
them, forming new products, and extract from them substances 



Fig. 14 



°oW °$° 



°0 
°0 



ooooo° 



oCi 






oro 



®§S^ © 



% 



% <„*o. *« -»» 



v Bff.S> 



Q?o # 



© 




c d e 

a, staphylococci; b, streptococci; c, diplococci; d, tetrads; e, sarcinse. (Abbott.) 

necessary to their growth and subsequent reproduction. The sub- 
stance in which they thus grow is called the medium or soil. The 
conditions under which this is accomplished are: (1) The fungi must 
have a proper vitality. (2) Their food-supply or soil must be suited 



MICROORGANISMS AS EXCITING CAUSES OF DISEASE 41 

to their growth and must be moist. When dried they may retain 
their vitality without development for mouths. In general terms 
they require water, CNO, and salts. (3) The temperature must be 
suitable; they grow more actively at about 102° ¥.•; at 160° F. 
maintained they usually die, but in some eases, as with the typhoid 
bacilli, they may live in the spore form at 
even 212° F. or over unless maintained for FlG - 15 

some time. Some that develop best at high ^>-i ^-^ _: 

temperature are called thermophilic. Low -^^--X^^^^ 

temperature, as 32° F. or far below that, /r^^-^'A^-^ -V : \ 
inhibits their growth, but does not neces- J '/y^r^l^^^y ■ 
sarily kill them. (4) Their w^aste products *"'"" <; <-*LV- :; 5>' 
must be removed or they die in them. Zooglea of bacilli. (Abbott.) 
This is said to be due to the reaction, 

whether acid or alkaline, and not to any of the other by-products — 
e. g., in lactic fermentation 2 per cent, of lactic acid is about the 
greatest amount endured by them. They are also sensitive to and 
inhibited by agitation, daylight, electric light, and electric currents. 
Morphologically the schizomycetes are grouped into several families 
according to form, methods of reproduction, and motion. The 
following is Migula's classification modified by McFarland: 1 

I. Family Coccacese. — Cells globular, becoming slightly elongate 
before division, which takes place in one, two, or three directions 
of space. Formation of endospores very rare. 

1. Streptococcus. — Division in one direction of space only, producing 
chains of organisms like strings of beads. No flagella. 

2. Micrococcus. — Division in two directions of space, so that fours 
or tetrads are often formed. No flagella. 

3. Sarcma.— Division in all three directions of space. Leading 
to the formation of bale-like packages of cocci. No flagella. 

4. Planococcus. — Division in two directions of space, like micro- 
coccus. Flagellated. 

5. Planosarcina. — Division in three directions of space, and like 
sarcina, but provided with flagella. 

II. Family Bacteriacese. — Cells more or less elongate, cylindric, and 
straight. Never form spiral windings. Division in one direction 
of space only, transverse to the long axis. 

1. Bacterium. — Without flagella. Occasional endospores. 

2. Bacillus. — Flagella arising from all parts of the surface. Endo- 
sporulation usual. 

3. Pseudomonas. — Flagella attached only at the ends of the cells. 
Endosporulation rare. 

1 Text-book of Pathology. 



42 MICROORGANISMS AS EXCITING CAUSES OF DISEASE 

III. Family Spirillaceae. — Cells spirally twisted like a corkscrew, or 
short and curved and representing segments of the spiral. Division 
transverse to the long diameter. 

1. Spirosoma. — Rigid.. Without flagella. 

2. Mwrospira. — Rigid. One, two, or three undulating flagella 
attached to the ends. 

3. Spirillum. — Rigid. From five to twenty semicircular or undu- 
lating flagella attached to the ends. 

4. Spirochete. — Serpentine and flexile. Flagella not observed. 
Movement probably accomplished by means of an undulating mem- 
brane. 

IV. Family Mycobacteriaceae. — Cells forming more or less elon- 
gate, cylindric filaments, often clavate-cuneate or irregular in form. 
Xo endospores, but formation of gonidia-like bodies due to segmen- 
tation of the cells. Xo flagella. Division transverse to the long 
diameter. Xot surrounded by a sheath as in chamydobaeteriaceae. 

1. Mycobacterium. — Cells in their usual form, short cylindric 
rods, often bent and irregularly cuneate. At times Y-shaped forms 
or longer filaments with true branchings. Sometimes produce 
short coccoid elements, perhaps gonidia. (This genus includes the 
corynebacterium of Lehmann-Xeumann.) 

2. Actinomyces. — Cells in their ordinary form occur as long 
branched filaments. Produce gonidia-like bodies. Cultures usually 
have a moldy appearance, due to the development of aerial hyphae. 

V. Family Chamydobaeteriaceae. — Vary in different stages of 
their development. Characterized by a surrounding sheath about 
both branched and unbranched threads. Division transverse to 
the length of the filaments. 

1. Cladothrix. — Characterized by pseudo-dichotomous branchings. 
Division only transverse. Multiplication by the liberation of whole 
branches. Transplantation by means of flagellated swarm spores 
which are actively motile. 

2. Crenothri.r. — Cells united in unbranched threads, which in 
the beginning divide transversely only. Later the cells divide in 
all three directions of space. The products of final division become 
spherical and serve as reproductive elements. 

3. Pharagmidiothrix. — Cells at first united into unbranched 
threads. Division in all three directions of space. Late in develop- 
ment, by the growth of certain cells through the delicate, closely 
approximated sheath, branched forms are produced. 

4. Thiothrix. — L^nbranched cells inclosed in a delicate sheath. 
Xon-motile. Division in one direction of space. Cells contain sulphur 
grains. 



MICROORGANISMS AS EXCITING CAUSES OF DISEASE 13 

VI. Family Beggiatoaceae. Cells united to form threads, which 
are not surrounded by an inclosing sheath. The septa are scarcely 
visible. Division transversely only. Motility accomplished through 
an undulating membrane. 

Beggiatoa. — Cells contain sulphur grains. 

Fig. 16 

*V *£ >' -$ 



a b c d 

a. Bacillus subtilis with spores: b, Bacillus anthracis with spores; c, Clostridium with 
spores; d, bacillus of tetanus with end spores. 

If in division the micrococci agglomerate like a bunch of grapes, 
without a definite arrangement in pairs, etc., they are called often 
staphylococci (staphle, a grape). During reproduction bacteria 
may excrete a material which unites them into a gelatinous mass 
called zooglea. Some, as the pneumococcus, form a gelatinous capsule 
about themselves, the office of which is not known. 

Fig. 17 
f I 







a b 

a, spirillum of Asiatic cholera (comma bacillus) ; b, involution forms of this organism 
as seen in old cultures. (Abbott.) 

The bacilli in the course of reproduction may form long threads, 
showing, as a rule, the traces of segmentation. Under certain un- 
favorable conditions of development a bacillus forms a glistening 
oval body within itself (endospore) which resists stains. The body of 
the bacillus may attenuate into a capsule for the spore. When the 
spore germinates this bursts open and the new bacillus escapes. 
These spores are very resistant to devitalizing agents. The bacilli- 
forming spores are said to be in the resting stage. These spores 
under favorable conditions again form bacilli like their progenitors, 
but do not form other spores without this return to the bacillus form. 
A single cell forms, as a rule, but one spore. 

If the entire bacterium is changed into the spore form they are 
called arthrospores; when cocci take on the appearance of spores 



44 MICROORGANISMS AS EXCITING CAUSES OF DISEASE 

they are also called arthrospores. Under unfavorable conditions 
bacteria may undergo degeneration and take on abnormal or involu- 
tion forms, and when the conditions are again favorable to develop- 
ment they may resume their typical forms. 1 While these form 
changes occur, bacteria are never permanently changed from one 
form to another. 2 Those bacteria which have several forms in their 
life cycle are termed pleomorphic. Those having but one form are 
monomorphic. Ptomains are products of decomposition of the 
medium and some are poisonous if taken in as food. Those bacteria 
which exist on living tissue are known as parasitic. They enter the 
body by way of open wounds or surfaces deprived of epithelium, 
or may lodge at certain points of the mucous surface of the lungs, 
skin openings, or the alimentary canal. If not killed out they multiply 
in the natural juices of the part on which they locate and produce an 
infective inflammation. Poisonous substances may be generated, 
which are absorbed into the system and may act as poisons, pro- 
ducing toxemia. When the toxin is soluble, diffuses from the bacteria 
and floats in the blood it is called extracellular toxin or exotoxin; 
when confined to the bacteria and liberated upon dissolution of the 
bacteria, it is called endotoxin; when the free toxin gives the reaction 
for albumin it is called a toxalbumin. 

The character of both the inflammation and the poisoning depends 
upon the particular bacterium or bacteria present. The bacteria 
may in certain cases be taken into the blood, and, coming to rest at 
certain spots, the above-described process is repeated. 

The Bacillus anthracis divides in the blood stream, 3 and other 
organisms, such as the Bacterium pneumoniae and Bacillus influenzas 
and the pyogenic organisms may exist in it. They may thus localize 
in a spot and produce effects. This has some significance in the 
production of blind apical abscesses and pericemental abscess (dental) 
and in the reverse general infection from dental sources. Many 
forms of organisms exhibit a preference for certain spots at which 
they find the conditions best suited to development — e. g., the typhoid 
bacillus in the glands of the ileum, Peyer's patches; the anthrax 
bacillus in the lungs of animals; the diphtheria bacillus in the 
mucous surfaces of the pharynx and contiguous parts. Bacteria 
may enter the blood via the mucosa of the alimentary canal, but 
this is ordinarily highly resistant. Those parasitic bacteria which 
produce disease are called pathogenic, others are non-pathogenic. 

1 Abbott, Principles of Bacteriology. 

2 The subject of transmutation when certain bacteria (as Streptococcus viridans) are 
gradually changed from anaerobic to aerobic conditions is now under study. 

3 Green, Pathology and Morbid Anatomy. 



FERMENTATION 45 

The mouth offers a suitable habitat for luauy bacteria. 

The bacteria which live on dead organic matter are called sapro- 
phytic (sapros, rotten, and phuton, a plant). They break up the 
dead animal and vegetable matter into simple compounds like 
carbon dioxid, ammonia, etc., which are utilized by the higher chlor- 
ophyllous plants. The nitrogen of the air is also utilized by some 
plant bacteria, and can be introduced to aid crops. As animals are 
dependent upon plants for existence, their vast importance in the 
economy of nature is evident. Bacteria may often pass from a para- 
sitic existence to a saprophytic one — a fact which is utilized in their 
study by bacteriologists, who prepare artificial media in which to 
cultivate them. These are called cultures, which by transference from 
one culture plate to another of like kind are said to be passed through 
generations. When by careful segregation one form of bacterium is 
separated from others present in a mixed culture and thereafter 
cultivated alone, it is called a pure culture; when the bacteria are 
thinly spread on a gelatin or agar culture and then isolated, the 
grouped bacteria developing at each point are called a colony. 
Bacteria may pass from a saprophytic to the parasitic form of exist- 
ence. Bacteria which have this power of adaptation to a new form 
of medium are called facultative. When without this power, they 
are obligate bacteria. 

According to Pasteur, those which develop in the presence of free 
oxygen as in the air are called aerobic. Those which cannot live 
in its presence are anaerobic. These derive the necessarj- oxygen 
from the medium. Those which live either w^ay are facultative. 
Those compelled to either mode of existence are obligate. 

When bacteria produce pigment either wdthin themselves or their 
medium, they are termed chromogenic; when they produce light or 
phosphorescence, they are termed photogenic. If they have the 
ability to produce fermentation, they are termed zymogenic; when 
they produce gas they are called aerogenic. 

FERMENTATION. 

Fermentation in the broadest acceptation of the term has been 
defined as the decomposition of substances possessing complex 
molecules under the influence of organized (living) or unorganized 
ferments (enzymes). The decompositions occur when organic sub- 
stances are exposed to the action of fungi or their enzymes, or are 
subjected to the action of certain ferments such as are found in the 
digestive fluids secreted into the elimentary canal, which are really 
enzymes also derived from living cells. 



46 MICROORGANISMS AS EXCITING CAUSES OF DISEASE 

According to Woodhead, 1 the molecules of the fermented compound 
are separated from one another for a brief period and then allowed to 
combine and form simpler and more stable compounds. The process 
is accompanied by heat due to chemical changes. 

Ferments, then, are of two kinds: (1) organized or formed fer- 
ments or living fungi which multiply at the expense of the sub- 
stance which they are fermenting; (2) unorganized or unformed 
ferments or enzymes, nitrogenous bodies produced by living cells 
which have the power of producing chemical changes in organic 
substances. They thus affect many times their own weight of the 
particular organic substance being fermented without being them- 
selves much affected, though eventually exhausted (catalysis). 
Typical examples are the pepsin of the gastric juice, which changes 
albumin to peptone, and the ferment of the yeast plant, proved 
capable of changing sugar into alcohol and carbon dioxid, even 
when the cells themselves are crushed and filtered out. 

The unorganized ferments usually act by oxidizing, deoxidizing, 
or hydrating the substance modified. They act best when their 
products are removed from the neighborhood. 

Many bacteria have been shown to possess such unorganized fer- 
ments. It is probable that they produce their effects on organic 
substances by the aid of these ferments, which serve them as pepsin 
serves man (extracellular ferments). It is thought that in other 
cases the germs take up organic food, digest it, and excrete waste 
products in somewhat the same manner that the body cells nourish 
themselves by intracellular ferments (p. 23). As a rule, more than 
one species of bacterium infects a fermentable substance. The 
more active varieties predominate in the fermentation, but mixed 
fermentations may proceed. In some cases the bacterial multipli- 
cation is favored by the activity of other bacteria (symbiosis), in some 
cases the development is retarded. Some may die out, finding an 
unfavorable soil. After a time the predominating bacteria may die 
in the waste products accumulated about them, leaving the field 
clear for a second or third variety. In this way progressive decom- 
positions may occur — e. g., the alcoholic fermentation may be suc- 
ceeded by the acetic, in which the alcohol is changed to acetic acid, 
as in cider-vinegar formation. The nature of the chemical changes 
produced in a fermentable substance depends upon the chemical 
nature of the medium and upon the nature of the fungus causing the 
fermentation. 

Thus, in an infusion of vegetable juices containing sugar a yeast 

] Bacteria and their Products. 



FERMENTATION 47 

fungus (one of the blastomycetes) will produce 1 carbon dioxid gas 
and alcohol if the oxygen of the air be freely admitted (aerobiosis) , 
while if to a fresh portion of the same solution scrapings from carious 
dentin be added, lactic acid will be formed, and, as a rule, no gas. 
Moreover, the reaction will occur if oxygen be excluded (anaero- 
biosis). In albuminous compounds an alkaline reaction and entirely 
different substances will be formed upon the addition of carious 
dentin. Probably upon this fact depend the different effects of 
bacterial plaques upon the teeth. (See Caries and Pyorrhea.) 

The ferments or enzymes produced by bacteria are quite numerous. 

Proteolytic ferments dissolve albuminous substances; proceed 
under an alkaline reaction and sometimes under an acid reaction. 

Diastatic ferments change starch into sugar. (See Dental Caries.) 

Inverting enzymes convert saccharose into dextrose or non- 
fermentable forms of sugar to fermentable ones. (See Dental 
Caries.) 

Coagulating ferments 'coagulate milk. Coagulation is also pro- 
duced in the tissues and exudate in inflammation by the ferments 
of pyogenic micrococci. 

Sugar-splitting ferments change sugar into other products, as 
alcohol, carbon dioxid, and lactic acid. 

Fat-splitting ferments split fats into glycerin and fatty acids. 

Hydrolytic ferments cause a combination with the elements of 
water in substances they decompose. 

Emulsifying, oxidizing, and nitrifying ferments also occur. 

Toxins are also classed w T ith the ferments, and are capable of 
producing new substances wdien distributed in the blood. (See 
Immunity.) 

Putrefaction. — The progressive decomposition of albuminous 
matter into simple compounds is effected by many bacteria through 
processes of oxidation, deoxidation, and hydration. 

Peptones 1 are first formed, next alkaloid-like bodies called pto- 
mains (putrefactive alkaloids); succeeding this such nitrogenous 
bases as leucin, tyrosin, and the amins (methyl, ethyl, and propyl- 
amin) are formed; next fatty acids and such acids as butyric, lactic, 
and succinic acid appear; next aromatic products such as indol, 
phenol, and cresol are formed, and the final decomposition is repre- 
sented in the end products — carbon dioxid, C0 2 ; hydrogen sulphid, 
H 2 S; ammonia, NH 3 ; and w T ater, H 2 0. When bacteria produce 
decomposition of living animal tissue they effect this putrefaction 
as distinctly noted in certain cases of abscess. 

1 Ziegler, General Pathology. 



is MICROORGANISMS AS EXCITING CAUSES OF DISEASE 

Such products of bacterial action, either produced in a living or 
a saprophytic medium, as are capable of acting as poisons in the 
animal organism are called toxins. Some animal parasites also pro- 
duce them. It is understood that they differ according to the fungus 
and the medium. If the toxin be proteid in nature, it is termed a 
toxalbumin. 

Some of the ptomains are toxic; the greater number are not. The 
poisoning due to the eating of putrefactive meats, fish, etc., containing 
them is known as "ptomain poisoning." 1 



Fig. 18 



Fig. 19 




Staphylococcus pyogenes aureus 
(micrococcus). From a culture. X 
1000. (Green.) 



Streptococcus pyogenes. From pus 
found in a pyemic abscess. X 1000. 
(Green.) 



When the toxins alone are absorbed from a focus of infection the 
subject is poisoned — a condition called toxemia, whether due to a 
toxic ptomain, as in the case of Asiatic cholera, or to a toxalbumin, 
as in the case of diphtheria. Such toxemia is commonly accompanied 
by more or less fever, according to the amount taken up. When the 
organisms enter the circulation and multiply in the blood, or at least 
move about and live in it, to be carried to capillaries in which they 
can rest and multiply, the condition is termed a septicemia. 2 In 
toxemia and septicemia the symptoms depend upon the nature of the 
organisms and their products. (See page 148.) Bacteria are found 
everywhere and exist upon the surface of the body, in its external 
cavities, and in the alimentary canal. Here under conditions of health 
there seem to be conditions favoring certain forms, which, when 
implanted, occupy the field and exclude, except temporarily, other 

1 For a table of origins, formula?, and toxicity of ptomains, see Gould's Medical 
Dictionary. 

2 Abbott, Principles of Bacteriology. 



FERMENTATIOh 49 

forms to which the soil is not so well suited. These are known as the 
"normal flora." It has been shown, however, that the growth of 
some bacteria is favored by the presence of certain others (symbiosis). 
This is said to be characteristic of Vincent's angina, in which the 
fusiform bacillus is symbiotic with a spirochetal form. 

After certain changes occur in the medium, other forms may become 
implanted. Pathogenic bacteria may exist in the healthy cavities 
and produce no ill results. Again, the soil may favor and disease 
begins. Certain bacteria have been found constantly present in 
relation with certain diseases — e. g., the spirillum of Asiatic cholera 
with that disease, the Treponema pallidum with syphilis; these are 
specific bacteria. Taken from individuals with the disease, they 
produce it in susceptible animals inoculated with them if circum- 
stances favor their growth. 

Fig. 20 



--It 






to* a 










'§% 



Mouse's lung; vessels plugged with Bacilli anthracis: a, alveolus; v, vein full of bacilli; 
c, capillaries also full; br, bronchus. X 400. (Horsley.) 



Bacteria spread in the tissues along the lines of least resistance. 
They may follow the cellular tissue or enter the lymphatics, or pass 
at once into the veins and be carried into the circulation. They may 
be strictly localized at the point of infection. 

Thus there may be a localized inflammation — e. g., in simple 
abscess due to the Staphylococcus pyogenes aureus; a diffuse inflam- 
mation, as in case of infection by the Streptococcus pyogenes; a 
gland infection or a septicemia, as in anthrax or in a general infection 
by Streptococcus pyogenes or Bacterium pneumonise; or a metas- 
tatic inflammation, as in pyemia, in which the germs (usually Strepto- 
coccus pyogenes) gain access to the blood from a local focus of infec- 
4 



50 MICROORGANISMS AS EXCITING CAUSES OF DISEASE 

tion and are carried to distant parts, in which they cause abscesses 
while the products produce toxemia. To produce effect, germs in 
the blood must come to rest at some point, which may occur in 
the capillaries owing to their injury, in thrombi or emboli, or, in case 
of entrance of bacteria into a leukocyte, they may migrate into the 
connective tissue (Fig. 20). 

It has been shown that pyogenic germs may exist in the blood 
without local effects, while again a local injury may cause the arrest 
of the germs and a secondary local inflammation or abscess be set 
up. This is due to simple arrest or to extravasation of blood, which 
permits the germs to pass from the vessels into the connective tissue. 

General or local depression of tissue vitality acts as a predisponent 
to local infection. 

The infections themselves are classified as primary, secondary, 
and mixed. 

The primary is the original infection, say, e. g., Bacillus tubercu- 
losis. The secondary is that implanted when the original disease is 
well under way — e. g., Streptococcus pyogenes aureus upon tuber- 
culosis; a third or tertiary infection is possible. 1 

The original infection may be by mixed germs, more than one of 
which may multiply. Thus, the Streptococcus pyogenes aureus and 
Bacterium pneumoniae may both be found in an abscess. This is a 
mixed infection. 

BACTERIA OF THE MOUTH. 

In even the best-cared-for mouths bacteria are numerous and find 
the conditions suited to their growth. In unclean mouths containing 
food debris, dead epithelium, etc., their life conditions are much 
more favorable. 

According to Miller 2 there are a number of bacteria which invari- 
ably occur in every mouth. These are: 

1. Leptothrix innominata. 

2. Bacillus buccalis maximus. ' 

3. Leptothrix buccalis maxima. 

4. Jodococcus vaginatus. 

5. Spirillum sputigenum. 

6. Spirochete dentium (denticola). 
To this list Goadby 3 has added: 

Leptothrix racemosa of Vicentini, further described by Williams. 4 

1 Park, Surgery by American Authors. 

2 Microorganisms of the Human Mouth. 

3 Mycology of the Mouth, 1903. 

4 Dental Cosmos, 1899. See Dental Caries. 



BACTERIA OF THE MOUTH 



51 



Streptothrix buccalis. 

Streptococcus brevis of Lingejsheim and Cladotlirix buccalis (pro- 
visionally added.) 

With the exception of Streptococcus brevis and perhaps Clado- 
tlirix and Bacillus buccalis maximus, these have been until recently 
uncultivable on laboratory media, and are strictly obligate parasites. 
Of the last-named organism, Goadby obtained biological character- 
istics of the pure culture, but he did not establish its disease-producing 
power, if it possesses any. Noguchi, 1 working in the Rockefeller 
laboratories, has cultivated several 
forms of oral treponemata (so-called 
spirocheta) by the use of ascitic fluid 
and fresh sterile tissue in the medium. 
(See Pyorrhea Alveolaris). 

Certain pathogenic organisms 
have been shown to be present in 
the mouths of healthy persons, 
such as bacteriological investigators; 
those nursing infectious diseases, 
such as diphtheria, scarlet fever, 
etc., and even in the mouths of 
healthy individuals apparently not 
exposed to any infection. In 
about 10 per cent, of all individuals 
examined at random, Netter found 
Staphylococcus pyogenes aureus 
(golden pus) . Staphylococcus pyo- 
genes albus was also found. The 

Pneumococcus, or Bacterium pneumoniae, was found in the mouths 
of about 15 per cent, of healthy individuals. This organism has been 
found by Kirk to be apparently causative of pericemental abscess, 
and has been reported by Schreier 2 as found in 75 per cent, of cases 
of apical abscess examined. It has also been related with cases of 
osteomyelitis and Ludwig's angina. The Bacillus diphtheria? of 
Loffler has been found in about 10 per cent, of mouths examined 
at random, and 33 per cent, of 600 children in a school examined 
during an epidemic of diphtheria were found to have the bacillus 
present in the mouth, while but about 2 per cent, developed the 
disease. 3 This latter fact shows the absolute necessity for at least 
a local predisposition as well as an exciting cause. 




Diplococci pneumoniae entangled in 
the meshes of the fibrinous exudation. 
From a section of lung in the "red 
hepatization" stage of acute pneu- 
monia. In the upper part of the field 
is a cell containing several cocci — 
possibly a phagocyte. X 1000. 
(Green.) 



1 Journal of Experimental Medicine, vol. xv. 
3 Goadby. 



2 Dental Cosmos, 1893. 



52 MICROORGANISMS AS EXCITING CAUSES OF DISEASE 

The Bacillus tuberculosis exists in the mouths of many suffering 
from pulmonary tuberculosis, and exists also at times in the mouths 
of the healthy. The Saccharomyces albicans may be present and 
at times produce thrush (Fig. 9). 



Fig. 22 




Bacillus diphtherise: A, its morphology on gly cerin-agar-agar ; B, its morphology on 
Loffler's blood serum; C, its morphology on acid blood-serum mixture. (Abbott.) 



The Bacillus typhosus (typhoid) has been found in the healthy 
mouth, and at times has oral pathogenicity. Many other organisms 
have been isolated from the human mouth. Some of these have a 
specific character, of others little is known. The mouths of pro- 
fessional nurses have been shown to contain bacteria, which increased 
the danger of infection of their patients, and that the sanitation of 
their mouths reduced the danger. Some of the bacteria of the mouth 
possess the power, under certain conditions, of felting themselves 
in plaques upon the surfaces of the teeth. Here, if properly supplied 
with carbohydrate food, some of them produce lactic acid and 
decalcify the teeth. Some bacteria have a later putrefactive action 
upon the organic matrix of the dentin. Some of the masses may 
develop an alkaline reaction due to putrefaction. Goadby 1 gives 
an interesting classification of bacteria found in dental caries (which 
see). Some bacteria not yet isolated are the probable causes of 
pyorrhea alveolaris. (See chapter on Pyorrhea Alveolaris). M. T. 



Mycology of the Mouth. 



THE RESISTANCE OF THE TISSUES TO INFECTION 53 

Barrett 1 has discovered an ameba constantly associated with pyor- 
rhea alveolaris. (See Pyorrhea Alveolaris.) 

The bacteria in the mouth probably are taken into the food and 
swallowed in great numbers. Many are doubtless killed by the gas- 
tric juice, which is a weak germicide; notwithstanding, some pyo- 
genic cocci and some of the blastomycetes may develop in the stomach 
and produce disease. Many also may enter the intestines and either 
excite disease of specific character or pro- 
duce abnormal intestinal fermentations, the FlG - 23 
toxins of which may be absorbed, and pro- x $&, \ 
duce malnutritional conditions. They may v '®f 
remain localized in the mouth and produce ' j*~>~ 
oral disease, dental caries, or pericemental I / 
diseases, etc.; abscesses, pyorrheas, etc., are ^ W&\ 
unquestionably the causes in many instances » ^*$ \ 
of fever, septic infection, intestinal disturb- / 
ances, endocarditis, pulmonary tuberculosis, „ .„ 

, . , , . . . . Bacillus tuberculosis. X 

glandular enlargements, joint inflammations 1000. (Green.) 

of rheumatic character, skin eruptions, etc. 

The relation of an unclean mouth to effects upon the mouth, ali- 
mentary canal and air passages and blood and lymph channels, is, 
therefore, a direct one of an importance that renders exact studies in 
this direction of extreme value. The saliva, while not germicidal 
(Miller), may or may not contain substances acting as pabulum for 
the growth of bacteria, but probably does in many cases apart from 
extraneous food materials introduced. It has been considered by 
Hugenschmidt that the saliva is positively chemotactic, attracting 
many leukocytes to the oral mucous membrane; also the great 
vascularity of the part probably aids in reducing effective inoculation. 

THE RESISTANCE OF THE TISSUES TO INFECTION. 

The resistance of the tissues to bacteria is to be considered from 
two main standpoints: (1) The prevention of the entrance of bac- 
teria into the tissues. (2) The destruction of the bacteria after 
entrance into the tissues. 

1. The prevention of entrance. It has been shown that pathogenic 
bacteria may enter the mouth, alimentary canal, lungs, etc., but few 
develop. 

.The skin acts as a mechanical barrier, though its openings may at 
times harbor bacteria. 

The mucous membrane secretes mucus, which envelops bacteria 

1 Paper read before the Pennsylvania State Dental Society and the National Dental 
Association, 1914. (See Dental Cosmos, August, 1913.) 



54 MICROORGANISMS AS EXCITING CAUSES OF DISEASE 



and with it they are carried away. The healthy mucus also has 
apparently a devitalizing power for some bacteria, not for others. 



Fig. 24 



7 







1, a spore which has penetrated the intestinal wall and entered the abdominal 
cavity, where four leukocytes have surrounded its end: m, the muscular layer of the 
intestine; e, epithelial layer; s, the serous layer. 2, a spore surrounded by leuko- 
cytes from the abdominal cavity of a Daphne. (Metchnikoff.) 

The acid gastric juice kills many, but some may pass through, two 
or three hours after a meal, at times when the gastric juice is not 

active. Probably the intestinal 
FlG - 25 juices also inhibit, in large de- 

gree, the action of such as have 
entered the alimentary canal. 
In all cases the agitation of the 
fluids of a part seems to act 
mechanically to prevent locali- 
zation of bacteria. 

2. The prevention of develop- 
ment in the tissues. Within the 
healthy tissues bacteria find 
several elements opposing their 
development. 

It seems the consensus of 
opinion among pathologists that 
the blood serum normally con- 
tains germicidal substances 
probably of the nature of a 
nuclein and called by Buchner 
"alexins." 

This belief is mainly based 
upon the demonstration of Nut- 
tall that filtered blood serum pos- 
sesses the power of producing the 
degeneration of bacteria. Buchner found that heating to 55° C. 
destroyed this property, a fact pointing to the albuminous nature of 
the alexins. After reviewing all the evidence, Vaughan and Novy 1 
conclude: 

1 Cellular Toxins. 




Active phagocytosis. Endothelial ceUs 
enclosing the bacilli of swine septicemia, 
from an hepatic vein of a pigeon: a, a, 
indothelial cells; b, b, leukocytes. 
(Metchnikoff.) 



THE RESISTANCE OF Till-: TISSUES TO INFECTION 55 

" (1) the exact nature of the germicidal constituents of the blood or 
alexins is not known; (2) the alexins have their origin in the white 
blood corpuscles; (3) disintegration of the white blood corpuscles 
liberates alexins; (4) it is probably true that alexins are also secreted 
by living leukocytes." Authorities disagree 1 , some claiming multi- 
plicity of alexins, others that only one alexin exists in a given serum 
(Metchnikoff). 

Metchnikoff, in 1884, demonstrated that the leukocytes take 
up bacteria within themselves and claimed that they thus destroy 
them. This process he termed phagocytosis {^hago, I eat; cytos, 
a bud). The polymorphonuclear leukocytes, called microphages 
by Metchnikoff, and the large mononuclear leukocytes, which he 
called macrophages, have this power. The macrophages take up 
dead leukocytes. It is now considered that this property, which 
is also possessed by the endothelial cells of the bloodvessels and 
serous cavities, is but evidence of the nutritive function of simple 
cells occurring after the bacteria have been partially degenerated 
by the serum (Fig. 25). This is borne out by experiments: Mixed 
pyogenic cocci and leukocytes free from blood serum exhibiting no 
phagocytic activity, whereas when the bacteria are first exposed to 
blood serum and then to phagocytes, there is marked phagocytosis. 
(See Opsonins.) In some cases bacterial disintegration may liberate 
the intracellular toxins and thus permit the toxic effects upon the 
host. This is said to be true in case of administration of typhoid 
vaccines during the course of the actual disease. 

Researches of Leber, Buchner, and others have shown that leuko- 
cytes may be attracted by certain bacterial products even in high 
dilution, and by other chemical substances such as mercury and 
copper salts. This is called positive chemotaxis. The opposite is 
negative chemotaxis. It has been shown that the negative may be 
followed by marked positive chemotaxis. 

Toxins are negatively chemotactic, and when bacteria produce 
much toxin phagocytosis and suppuration are lessened, 1 e. g., in 
streptococcus infection. Many other bacterial products and bac- 
terial proteins are positively chemotactic, and when they are pro- 
duced in place of much toxin phagocytosis is increased, and the 
bacteria, if few, are coincidently destroyed by the alexins and taken 
up by the phagocytes with resolution, or, if the bacteria be numerous, 
suppuration is increased and the bacteria expelled as a protection 
to, the body. It has been shown, however, that the taking up of 
living bacteria may occur and may spread an infection. Also it has 

1 Stengel, A Text-book of Pathology. 



56 MICROORGANISMS AS EXCITING CAUSES OF DISEASE 

been shown that the microphages take up some bacteria and the 
macrophages take up others. 

If the combined local forces be incompetent to kill out the infecting 
organisms, the local infection spreads until limited or the patient 
dies; or a metastasis may occur, in which case the process is prac- 
tically repeated in another locality. 

IMMUNITY. 

Immunity is the opposite of predisposition, or susceptibility, 
and may be defined as that condition of the local fluids, the blood, 
or the body cells, in which inoculation with bacteria or bacterial 
products has no injurious effects. 

There is also some relative immunity to non-infectious diseases, 
e. g., females to hemorrhagic diathesis. (See Predisposition p. 30.) 
Immunity to infective agencies may be natural or acquired. 

Natural Immunity. — This is due to a healthy action of the phago- 
cyte of the body or to some peculiar substance in the blood; the 
antibody of the particular bacterium, or fungus or toxin which it 
is thought may be inherited from ancestors. 

Typical examples of this kind of immunity are those of the rat to 
dphtheria; man to rinderpest; lower animals to syphilis; the negro 
to yellow fever (though he is susceptible to smallpox) ; the hog to 
snake venom, etc. 

Natural immunity may change to susceptibility through some 
change in the systemic condition. Thus, two students attending a 
scarlet-fever ward for months became susceptible through the effects 
of a long walk and hunger; both took the fever, one dying. 1 

Rats, run in a wheel until exhausted, were successfully inoculated 
with anthrax bacilli, to which they are normally insusceptible. These 
states of tissue fatigue are noted in the overstrain of athletes, who 
often suffer from furuncle. According to Gilder sleeve 2 examination 
shows that the opsonic index is greatly lowered by the overstrain. 
Metchnikoff considers immunity due to an enzyme derived from the 
leukocytes called microcytase, which either acts within the leuko- 
cytes or outside of them to produce deterioration of the bacteria 
(cytolysis), and that it may require other factors to act with it as 
amboceptor or complement. 

Natural immunity may therefore fail upon severe test, and 
survival of the test is the only certain assurance. This natural 
immunity may be of two kinds : 

1 Green, Pathology and Morbid Anatomy. 2 Lecture. 



IMMUNITY 57 

1. Natural toxin immunity, e. g., hog to snake venom. 

2. Natural bacterial immunity, e. g., negro to yellow fever. 
Acquired Immunity.— This is of two kinds: 

1. x\cquired toxin immunity. 

2. Acquired bacterial immunity. 

Acquired Toxin Immunity. — Toxin immunity may be acquired in 
two ways: 

1. By the injection of small doses of toxins at intervals until no 
reaction results. The horse is so immunized in diphtheria antitoxin 
production. The antitoxin is produced by the cells of the horse. 

2. By the injection into man or animals of serum containing anti- 
toxin produced by method No. 1. The former is an active immunity; 
the latter passive. 

Acquired Bacterial Immunity. — Immunity to bacterial inoculation 
may be acquired in several ways : 

1. Naturally, through having had an attack of the particular 
specific disease; thus, as a rule, measles, smallpox, syphilis, yellow 
fever, and many other infectious diseases cause the body cells to 
produce substances antagonistic to the bacteria known as anti- 
bodies which are said to be in part the cause of immunity. Phago- 
cytosis is increased against subsequent infections which remain in 
the blood and render the individual immune to a second attack, 
though in some cases this immunity is lost. 

2. Artificially, through the injection into the body of attenuated 
bacteria, cultivated through several generations under unfavorable 
conditions; for example, at increased temperatures or in the presence 
of weak antiseptics or by passing them through other animals, 
whereby their virulence is lost; a mild immunizing attack ensues. 
Thus in rabies, or, rather, for prevention of rabies, after the bite 
of an animal suffering from it, accurately graduated doses of emul- 
sions of the spinal cord of infected rabbits, dried for varying periods 
to produce accurately degenerated rabies germs, are injected into 
man, preventing the development of the germs introduced by the 
bite. The emulsion of older cords are injected first, then those of 
younger cords (dried for a shorter time) . The use of cowpox vaccine 
against smallpox is of this nature. 

3. Artificially, by the injection of dead bacteria from a pure culture 
of the specific bacterium from which immunity is sought. (Wright's 
vaccine.) What is known as the opsonic index is raised, and the 
person becomes more resistant to that particular infection; that is 
to say, phagocytosis is increased. (See Opsonins.) 

4. Artificially, by the injection of graduated doses of toxins, pro- 
duced in a saprophytic medium by the specific bacterium, all bacteria 



58 MICROORGANISMS AS EXCITING CAUSES OF DISEASE 

being filtered out. This is most readily done when the toxins pro- 
duced lie in the medium external to the bacteria (extracellular toxins). 
The horse is so treated in the production of diphtheria antitoxin for 
use in the diphtheria of man. 

5. Artificially, by the injection of the serum of animals immunized 
by method No. 4, which serum contains a substance antagonistic to 
the specific toxin and known as an antitoxin. Thus the injection 
of horse serum containing antitoxin of diphtheria produced by 
method No. 4 into a diphtheric patient aborts the disease by antago- 
nizing its toxin while the phagocytes kill out the bacteria. Injection 
into the attending nurse produces immunity to the disease, but 
antitoxin does not act upon the bacteria but upon the toxin. The 
immunity then is probably due to phagocytosis and an amboceptor 
which aids it. 



Fig. 26 



Fig. 2< 




A, complement; B, ambo- 
ceptor; C, receptor; D, part 
of cell. Showing how comple- 
ment destroys bacteria through 
the agency of amboceptors. 



e—-o^ 




-•r 



Cell with different kinds of receptors: C, 
receptors. The dark objects represent food 
molecules, toxins, etc. 



The methods 1, 2, 3, and 4 produce a much more lasting immunity, 
as the antagonizing substance is the result of cell reaction on the 
part of the individual, and is called active immunity; that produced 
by method No. 5 is passive immunity, because not produced by 
cell reaction, but directly introduced into the blood, and is much 
less lasting. It is not effective for all bacteria. 

The various forms of acquired immunity are explainable by the 
now generally accepted theory of Ehrlich known as the side-chain 
theory. 



IMMUNITY 59 

Ehrlich's Side-chain Theory. -This theory is based upon certain 
demonstrated facts and upon the supposition that each cell is com- 
posed of aggregations or groups of atoms and surrounded by side 
groups of atoms (molecules), which compose the cell protoplasm. 
Each atom group is supposed to have its own chemical affinity for 
food elements, poisons, etc., as shown by the selective affinity of 
drugs. 

These chemical atom groups, therefore, have a receptive function 
and are called receptors on the cell. Other groups have a fermenta- 
tive action and chemically change the substances presented; these 
are called zymophorous atom groups. 

Each toxin molecule has an affinity for some cell receptors, other- 
wise no effect is produced by it. (Snake venom has no effect upon 
the hog.) 

The receptor is considered to possess a group of atoms suited to a 
prehending action, whereby it combines with the toxin molecule (or 
food molecule in nutrition), which possesses a similar combining 
group of atoms. In each these are termed the haptophoroiis group. 
The toxin molecule is capable of inflicting injury upon or stimulating- 
cell action, as shown in the case of tetanus, in which tonic muscular 
contractions are excited. The group of atoms in the toxin mole- 
cule which accomplishes this is termed the toxophorons group 
(Fig. 27). 

That the body cells neutralize the toxin if not in overwhelming 
quantity is shown by the experiment of Wassermann and Takaki, 
in which a mixture of brain emulsion and tetanus toxin w r as inert 
when injected into a susceptible animal. Therefore, a zymophorous 
group of atoms is said to exist in the cell or its receptor. 

The Theory of Toxin Immunity. — The toxin produced during an 
infective disease, such as diphtheria, and floating in the blood, 
presents itself to cells for some receptors of which it has an affinity. 
The haptophorous atom group of its molecules joins with the hapto- 
phoroiis atom group of the receptor. The toxophorous atom of the 
toxin group exerts its action upon the receptor and is neutralized by 
the zymophorous group of the latter unless the toxin is in too great 
quantity. The cell, in case of injury, repairs itself by forming an 
excess of the particular kind of receptors having affinity for the partic- 
ular toxin. These receptors become detached and float in the blood, 
and there have the same affinity for the toxin. These are called 
receiptors in the blood, and constitute what is known as antitoxin. 
They are known to be formed by the body cells and not by the blood, 
as they have been found in the tissue juices of blood-making organs 
immediatelv after the introduction of toxin, while at the same time 



60 MICROORGANISMS AS EXCITING CAUSES OF DISEASE 



not found in the blood, though they afterward appear, as might be 
expected (Fig. 28). 

The antitoxin receptor (with affinity for the toxin molecule) has 
an haptophorous atom group which combines with the haptophorous 
group of the toxin molecule, which, having found its affinity in the 
blood, is satisfied, does not further affect the cells proper, and thus 
cell injury is prevented. This occurs naturally in each case of 
diphtheria, and probably recovery or death is dependent upon the 
ability of the body cells to furnish (1) antitoxin sufficient to antagonize 
the toxin and (2) another body to be described which antagonizes the 
bacteria. 



Fig. 28 



Fig. 29 





Showing separation of antitoxins, and 
combinations of toxins (dark) with free anti- 
toxins in the blood. 



-•/> 



Showing the action of anti- 
complement: A, complement; B, 
intermediary body; C, receptor; 
D, cell; E, anticomplement. 



In the case of diphtheria-serum therapeutics, the horse is com- 
pelled by method No. 4 to form these antagonizing substances, and 
the serum is then injected into the individual suffering an attack 
or threatened, thus furnishing him ready made the antagonizing 
substances (antitoxin, etc.). A special antitoxin is supposed to be 
formed for each kind of toxin. Ehrlich believes an antitoxin mole- 
cule to be capable of satisfying 200 toxin molecules, and that they 
combine chemically. In old sera the toxin undergoes a chemical 
change into toxoid, and the injection of this causes an increase of 
receptors on the cell, and thus renders the animal more susceptible 
to the action of the toxin. An antitoxin unit is the amount of 
antitoxin necessary to neutralize an arbitrary amount of a particular 
toxin. 



IMMUNITY 61 

Toxon is a third body produced by the bacteria which has some 
affinity for antitoxin, but the combination is still somewhat toxic 
(has a different toxophorous group of atoms), and in diphtheria is 
credited with the production of postdiphtheric paralysis. The 
attempt to make antitoxins has not been successful in most cases. 

The Theory of Acquired Bacterial Immunity. — When bacteria enter 
the tissue of an animal by inoculation and are not destroyed by the 
alexins and phagocytes, they develop and produce toxins and may 
themselves enter the blood. A reaction of the body cells occurs, as 
shown by fever, and not only antitoxin, but a new body is pro- 
duced by the cells, which, with the aid of still another substance 
called complement, is capable of destroying the particular bacterium 
causing the infection. This body is another form of receptor having 
two haptophorous groups, by which it links the complement with 
the receptor of the bacterium, and thus enables the complement to 
destroy the bacterium through its zymophorous atom group. The 
doubly haptophorous receptor is called from this fact the amboceptor 
(also intermediary or immune body) (Fig. 26). A different ambo- 
ceptor is produced for each bacterium and the host is immunized 
against this bacterium only. 

The complement, of which there are several in association in the 
blood (Ehrlich), is probably produced by the leukocytes, and is 
classed among the alexins. As stated, it has a zymophorous atom 
group, and also has an haptophorous atom group with which it 
joins the amboceptor. The complement is destroyed at 55° C. (is 
thermolabile). The amboceptor requires a higher heat (is thermo- 
stabile). 

In natural bacterial immunity it is thought that some of the 
amboceptors are inherited from immune ancestors, and that they 
exist together with complement in the blood ready to act. Metchni- 
koff claims that amboceptor and complement are products of the 
leukocytes. The elements in blood serum which destroy bacteria 
are termed bacteriolysins , and the new bodies formed by cells as a 
protection are called antibodies. 

Agglutination. — When body cells react to infection, and attempt to 
or effect immunity, the blood plasma may acquire the property of 
clumping the bacteria together, and they settle to the bottom of a 
test serum, leaving the fluid clear. It is supposed to be exhibited 
only toward the bacterium causing the infection, but experimentally 
out of the body {in vitro) others are sometimes affected. 

The substance producing agglutination, called agglutinin, evi- 
dently exists in blood as the result of cell reaction. It is of the 
nature of liberated amboceptors, but has a zymophorous group. It 



G2 MICROORGANISMS AS EXCITING CAUSES OF DISEASE 

therefore acts by combining by an haptophorous group and acting 
through a zymophorous group. 

The reaction is useful in making an early diagnosis of the kind of 
existing infection. Thus if typhoid bacillus be suspected as a cause 
of disease present and be the cause, the blood serum drawn from the 
patient will agglutinate living typhoid bacilli placed in it. This is 
known as Widal's reaction. 

Precipitins. — A substance of nature and origin similar to agglutinin 
causes precipitation instead of agglutination. It is used in diagnosis 
and in differentiating the blood of animals, a matter of importance 
in murder cases. 

Opsonins. — Wright found that when bacteria were mixed with 
leukocytes in the absence of serum phogocytosis did not occur, but 
if serum was then introduced it did occur. Also if leukocytes were 
washed with sodium citrate-chlorid solution to free them from serum, 
and bacteria that had been previously treated with serum were 
introduced, phagocytosis occurred. Obviously, then, the serum con- 
tains a substance or substances capable of favoring phagocytosis. 

It is regarded that this substance prepares the bacteria for the 
phagocytic process, and from this fact Wright named these sub- 
stances opsonins, which are therefore classed among the alexins. 
Opsonins have an haptophorous group of atoms prehending the bac- 
teria and a zymophorous group acting upon them. Other observers 
have determined that opsonins are multiple in normal blood. The 
degree of activity of the opsonin related to a particular infection when 
compared with that of a healthy person is called the opsonic index. 

The Opsonic Index. — To test the opsonic index, an even 
emulsion of the bacteria, the serum of the infected patient, the 
serum from each of several healthy persons, and healthy leukocytes 
from the healthy persons are necessary. 

1. The Emulsion. — The pure culture is isolated. A 2 per cent, 
nutrient agar medium has sterile milk, milk serum, or blood serum 
added in the proportion of 1 part to 3 of the nutrient agar. In 
tubes of the selected medium slant cultures are made, and incubated 
at 37.5° C. for eighteen to twenty-four hours. (Gildersleeve.) These 
are then washed from the surface of the medium with 0.85 per cent, 
sodium chlorid solution and the solution placed in a sterile bottle 
with sterile glass beads or sand and shaken to remove clumps. 
The number of bacteria in each cubic centimeter is then estimated 
(standardized) and a dilution made on the basis of this estimated 
count with 0.85 per cent, sodium chlorid solution, so that when 
opsonized with normal serum each leukocyte will take up from 5 to 
8 of ordinary bacteria. (Gildersleeve.) 



IMMUNITY 63 

2. The Sera. — These are obtained from the patient and healthy 
persons by congesting the finger with a rubber band and bleeding 
into a capsule or pipette, which is then sealed and the blood allowed 
to clot in the incubator for 15 to 20 minutes. 

The leukocytes are obtained by filling with blood a centrifuge 
tube, three-fourths full of a 1 per cent, solution of. sodium citrate 
in 0.S5 per cent, solution of sodium chlorid. After shaking, the 
tubes are centrifugalized, the fluid drawn from the buft'y coat, and 
the latter then carefully pipetted and drawn in and out to mix 
thoroughly. 

The preparations being ready, equal volumes of bacterial emulsion, 
the serum to be tested, and leukocytes are drawn into a marked 
pipette, each volume being separated by a bubble of air. These 
are then mixed by drawing in and out, and the end of the pipette is 
sealed and the pipette placed in an opsonizer for fifteen or twenty 
minutes. The pipette end is then broken, and the contents spread 
evenly on several glass slides by means of another slide. (Gilder- 
sleeve.) 

These are then air dried and stained. The bacteria in a given 
number of leukocytes are counted and the total divided by the 
number of leukocytes counted, thus obtaining the average of bac- 
terial ingestion per leukocyte. This gives the phagocyting index for 
the infected individual. 

The same procedure exactly is carried out with the normal sera, 
and the average phagocyting index determined. The index is cal- 
culated by dividing the patient's phagocyting index by the normal 
phagocyting index, or the same thing may be done by the following- 
proportion : 

Normal index : patient's index :: 1 : x. 

If x is above 1, the patient's index is high. 

If x is below 1, the patient's index is low r or subnormal. 

Vaccine Therapy. — Wright found that when a large number of the 
bacteria causing the infection were killed and then injected into the 
patient, their bodies contained substances which produced a cell 
reaction resulting in an increase of opsonin and phagocyting power 
in the leukocyte of the individual— this determined by the opsonic 
index. 

For a time — twenty-four or forty-eight hours — the index became 
lower. This Wright called the negative phase; afterward it gradually 
rose to a maximum. This stage he termed the positive phase. The 
object sought, then, is to increase the resistive power of the patient 
to the infection through an increase in the phagocytosis. 



64 MICROORGANISMS AS EXCITING CAUSES OF DISEASE 

The Vaccine. — This is prepared by producing an emulsion of the 
pure culture as for the opsonic index. The emulsion is then stand- 
ardized by an estimation of the bacteria in each cubic centimeter. 
The bacteria are then killed by heating the sealed container in a 
water bath and are then diluted with 0.85 sodium chlorid solution 
(with 0.2 per cent, of tricresol or phenol added) to the desired 
strength. 

The proper number of bacteria for one maximum dose should be 
contained in 1 c.c. of the diluted emulsion. To determine the dilu- 
tion the estimation in 1 c.c. of standardized emulsion is divided by the 
number desired as a dose, and the quotient less 1 equals the number 
of c.c. of the diluting solution to be added to 1 c.c. of the emulsion. 

The Injection. — The hypodermic syringe is sterilized and filled 
with the diluted emulsion and an injection made into a convenient 
site, which should be previously sterilized with 2 per cent, phenol 
solution, followed by sterile water and absolute alcohol (Gildersleeve) . 
The needle should be inserted into the subcutaneous tissue of the 
outer side of the arm, or, if preferred, of the leg or thigh, or below 
the angle of the scapula, whichever would prove most convenient for 
the purpose. 

Gildersleeve 1 recommends smaller doses when the index is low, in 
general infection, in acute conditions, in children, and in individuals 
markedly depressed, than in the opposite conditions. He gives the 
following dosage of the various vaccines employed in treating 
infections of the oral cavity: 

Micrococcus aureus and albus 50,000,000 to 600,000,000 

Streptococcus pyogenes 10,000,000 to 100,000,000 

Pneumococcus 10,000,000 to 100,000,000 

Micrococcus catarrhalis 25,000,000 to 100,000,000 

Influenza bacillus 25,000,000 to 100,000,000 

The Reaction of the Blood. — According to Michaels 2 (following 
Gautrelet), individuals in whom the oxidations are below normal, 
and who have a tendency to arthritic diseases because of an excess 
of the acid constituents or waste products in the body fluids, are 
denominated hyperacid individuals. The hyperacid have oxidations 
above the normal, together with a superabundance of saline chlo- 
rids; and these he regards as more subject to infection. There are 
three ways in w T hich the predisposition of the hypoacid might be 
accounted for: 



1 American Text-book of Operative Dentistry. This article should be read for a 
more extended description. 

2 Sialosemiology. 



EXTERNAL ANTIBACTERIAL INFLUENCES 65 

1. The increased amount of alkaline elements may permit an 
increased alkalinity of the blood, rendering it favorable to bacteria 
as a culture medium. 

2. The systemic change may introduce a substance into the 
blood which is a suitable pabulum for the bacteria, as, for example, 
excess of glucose in diabetes (according to Kirk 1 this occurs in the 
saliva in those susceptible to caries). 

3. Certain immunizing substances, opsonins, alexins, etc., may 
fail to be formed. 

Per contra, the hyperacid may be immune for opposite reasons. 
Whether this be a rational explanation or not, it is certainly shown 
by Wright that therapy will increase the opsonic index, and it 
may be that in the hyperacid the continuous cell irritation by the 
acid elements, as C0 2 , uric acid, etc., may cause a tissue reaction 
increasing alexin or opsonic power. 

The foregoing is merely a synopsis of the main facts governing 
immunity. There are many details which are omitted and for 
which the reader is referred to works on bacteriology. 

EXTERNAL ANTIBACTERIAL INFLUENCES. 

Many chemical substances and physical forces prevent the growth 
and reproduction of bacteria without necessarily killing them; these 
are called antiseptics; a weak solution of boric acid is an example, 
agitation is another, dryness another. Low temperatures also pre- 
vent fermentation. Other substances or forces kill the bacteria after 
an exposure to their influence for a sufficient length of time; these 
are germicides — e. g., a 1 to 1000 solution of mercuric chlorid in 
water, boiling water, or streaming steam; sunlight for some bacteria. 
Other substances destroy both the bacteria and their products ; these 
are disinfectants — e. g., sodium dioxid or other substances liberating 
nascent oxygen. Formaldehyde and iodin are also disinfectant. 

1 Dental Brief, 1907. 



CHAPTER IV. 

DISTURBANCES OF NUTRITION. 

Disorders of nutrition are of three classes: (1) due to an excess 
of nutritive material of all classes, or of one class; (2) due to a 
deficiency of nutritive material, active or relative; (3) due to the 
presence in the blood of material which, instead of serving the 
purpose of metabolism, disturbs it; (4) an inability of the cells to 
appropriate a proper quantity and quality of food. 

EXCESS OF NUTRITION; HYPERNUTRITION. 

An excess of nutrition may be either general or local. If local, 
it is associated with an overfulness of the bloodvessels (hyperemia). 
If the individual possess a general richness of blood, he is said to be 
plethoric. Sthenic plethora is such a richness associated with activity 
of the circulation and a consequent increase of the vital processes 
due to plentiful cell nutrition, and with an active repair of even 
excessive waste of cell protoplasm. 

In asthenic plethora, on the contrary, the individual is full-blooded, 
but the circulation is sluggish; waste products are probably accumu- 
lated in the blood and the vital processes are sluggish in consequence. 
Instead of the rich color and active movements associated with 
sthenic plethora, the asthenic have a purplish appearance and the 
movements are more labored. 

Local Hypernutrition. — An increased stimulation of the nerves of 
a part invites more blood to it, which within certain limits increases 
the nutrition to the cells of the part. This results in increased irri- 
tability, contractility, and general functional activity of the func- 
tionating cells. If this be maintained, the cells grow or multiply, or 
both, and the part is enlarged and capable of an increased amount 
of work. 

Stimulation beyond this point causes irritation or overstimulation 
of cells, and the vital processes become fretful; incomplete chemical 
changes occur in the cells, and the functional activity is disordered. 
The cells are wearied, and if the overstimulation be continued 
paralysis from overwork results. 
(66) 



EXCESS OF NUTRITION; IIYPERNUTRITION 67 

Hypertrophy.— Though strictly meaning an excess of nutrition, 
this term signifies an increase in the size of a part as the result of 
stimulation and destruction, with a compensatory rebuilding of 
cell material in excess (a cell hyperplasia) (Weigert 1 ). The new 
growth must be practically normal in structure. As a rule, both the 
size (simple hypertrophy) and the number of the cells (numerical 
hypertrophy or hyperplasia) are increased. The caliber of the 
bloodvessels is increased to comply with the stimulus to their 
controlling nerves — the vasomotors. Hypertrophy is frequently 
exhibited in tissues subjected to an unusual amount of work short 
of marked fatigue. An increase in its function occurs; its capacity 
for work becomes greater, and if the strong stimulus (mild irritation) 
implied be continued the cells increase in size and it may be in number, 
all three phases of the expenditures of an increase of vital energy 
being represented — functional, nutritive, and reproductive. If the 
heart be subjected to an increase in the strain ordinarily brought 
upon it, an increase in the volume of the muscular fibers follows, 
causing hypertrophy of the walls. The same is true of the muscles 
of the gravid uterus, in which the cells increase to many times their 
normal length. When one organ, as a kidney, takes up alone the 
work usually performed by two it increases in size (hypertrophies). 
This is called compensatory hypertrophy. It may occur in an organ 
which endeavors to supply the deficient function in another organ 
of different sort. Hypertrophy also occurs in many inflammatory 
conditions, and is due to the area of hyperemia surrounding every 
focus of inflammation. Thus the epithelium about the edges of an 
ulcer may thicken or new bone may be formed about an area of 
inflamed bone tissue or periosteum. The bone tissue may become 
more compact, a condition termed sclerosis of bone, as it results 
in the formation of formed (intercellular) tissue at the expense of 
the cellular elements. 

The removal of an accustomed resistance often produces an irri- 
tation resulting in mild hyperemia, and thickening or hypertrophy 
results — e. g., non-occlusion of teeth frequently produces hyper- 
cementosis. 

A form of cellular hypertrophy appears to occur in certain leuko- 
cytes, resulting in the formation of a multinucleated cell or "giant 
cell." 

Under irritation the nucleus subdivides, but the cell body fails of 
division, and instead of complete reproduction a large cell with many 
nuclei is formed (Fig. 30). These giant cells appear where tissue is 

' 1 See Abbott's Principles of Bacteriology, p. 601, for an amplification of this idea. 



68 



DISTURBANCES OF NUTRIT/OX 



to be removed, as in the case of aseptic foreign bodies or the roots 
of deciduous or even of permanent teeth. (See Resorption of 
Temporary Teeth.) An hypertrophy or excessive development may 
occur during intra-uterine life and is spoken of as congenital hyper- 
trophy. A low grade of inflammation may lead to a numerical 
hypertrophy, as in the case of hypertrophy of the dental pulp 
(which see). 

Hyperplasia. — Hyperplasia, sometimes called false hypertrophy, is 
an increase in size partly due to an increase in the number of the 
cells, though the individual cells may be smaller than normal. It 
occurs mostly in the connective tissues, though it ordinarily plays 
a part in most hypertrophies. The part is usually asymmetrical. 
Examples: elephantiasis and hyperplasia of the dental pulp. 

Fig. 30 




Dog's hair encapsulated in subcutaneous tissue: a, hair; b, fibrous tissue; c, pro- 
liferating granulation tissue; d, giant cells. Preparation hardened in alcohol, stained 
with Bismarck brown, and mounted in Canada balsam. X 66. (Ziegler.) 



Cyst and Tumor Formation. — A cyst is an enlargement contain- 
ing a cavity which in turn contains liquid, gelatinous, or pultaceous 
material, about which is a capsule condensed from the surrounding 
structures. The accumulation of the fluid or semifluid contents 
produces the enlargement of the part even if bony (Fig. 31). 

They differ from tumors in being strictly localized, though they 
may be large, and in their generally benign character, though tumors 
may at times have a cystic character. 

Cysts may be formed by the retention, secretion, or extravasation 
of fluid in several ways: (1) By the retention of normal secretion of 
a gland owing to the obstruction of its duct — e. g., ranula. These 
are called retention cysts. (2) By abnormal secretion into ductless 
cavities — c. g., bursse (exudation cysts). (3) By the extravasation 
of Jblood into a ductless cavity (extravasation cyst). (4) Indepen- 
dently in tissue as a result of mucoid or fatty changes or liquefaction 
necrosis, the surrounding tissue becoming condensed into a capsule 
(liquefaction or colliquation cysts). (5) Independently as a collection 



l-:.\( ESS OF NUTRITION; HYPEtlNUTRITION 69 

of fluid in connective-tissue spaces, which enlarge and (ill. The 
surrounding tissue condenses into a cyst wall. (6) Independently as 
a result of chronic irritation by foreign bodies, extravasated blood, 
or parasites, as in dentigerous cysts 1 (Fig« 31). Cysts may have but 
one cavity (simple cysts) or have numerous intercommunicating 
cavities known as loculi (compound or multilocular cysts). Forming 
within bony walls, these may be largely distended, and the walls 
are usually thin. There is generally a crackling sound produced upon 
pressure. Dentigerous and other cysts are usually lined by epithe- 
lium peculiar to the part. The explanation of Malassez, that epithe- 
lial remnants (of the enamel organs) develop, forcing the connective- 

Fig. 31 




Cyst of the lower jaw. having its origin about an undeveloped tooth. (Garretson.) 

tissue elements outward as a covering to them, is probably the correct 
one. Meanwhile, fatty degeneration of developed epithelium and 
the collection of fluid account for the fluid or pultaceous character 
of the cyst contents. This proliferation of epithelial remnants is 
well proved by the development of epithelial products in the interior 
of dermoid cysts. (See Fig. 98.) 

Dermoid cysts are cystic tumors of widely varying sizes found in 
various parts, such as the ovary, neck, base of brain, orbit, etc. 
They contain fatty and epithelial debris, and are lined with epithe- 
lium, outside of which is a corium with its papillae, and outside of 
this subcutaneous adipose tissue. The whole is inclosed in a fibrous 
capsule of connective tissue. The epithelial lining may contain 



70 



DISTURBANCES OF NUTRITION 



and develop the characteristically dermoid structures, hair, teeth, 
sebaceous and sweat "lauds (Fig. 34). 

Broomell 1 states that the hair is often several feet long, usually 
of a light brown color, regardless of the color on the outside; of the 
body, and becomes white as age whitens the outside hair, and is 
usually absent in dermoids in bald persons. Hair follicles are present. 

He states: " Dermoids of the mouth are usually found in the hard 
and soft palates, infrequently in the former, but when found are 
complicated, while the more frequently found in the soft palate 



Fig. 32 




Longitudinal section of a tooth from an ovarian cyst: a, b, d, tissue filling absorp- 
tion cavities; c, narrow band of connective tissue through which the organ a received 
its nourishment; d, absorption of enamel. (Miller.) 

are simpler. In these situations they range from the size of a pea 
to that of a hen's egg, the larger being pendulous. They are also 
found on the floor of the mouth and dorsum of the tongue. Brown 
instances a case in which one lay under the jaw and extended down 
the sid,e of the neck. 2 

"The teeth range in shape from the simple cone to multicusped 
complex forms, the crowns of the same being well formed. The 



Dental Cosmos, 1905. 



Ibid., 1908. 



DERMOID CYSTS 



71 



roots arc usually not fully calcified or developed, or, perhaps, partly 

be smooth 



ie eiianu 



1 in 



developed. A follicular wall is present. T 

or pitted. 

"The ceinentuni is usually absent or hut slightly developed. 

" Radicular odontomes evidenced by tiuuor-like growths on roots 
are due to aberration of the dentinal germ. The pulp canal was 
always present in cases examined. Fusion of teeth has occurred in 
these cysts. In histology the teeth are similar to ordinary teeth, 
with some slight aberration due to the peculiar condition." 



Fig. 33 




Absorption tissue, from cavity a in Fig. 32. 

According to Eccles and Hopewell-Smith/ the teeth may be found 
imbedded in alveoli in bone; that a small jaw with normal-sized 
teeth may exist. 

Miller 2 states that the cystic contents include fatty acid, oxalic 
acid, large quantities of tyrosin and leucin, which substances furnish 
the acid for the decalcification of teeth occasionally found, but that 
no bacterial action, such as occurs in the second stage of dental 



Proceedings of the Royal Society of Medicine. 
Dental Cosmos, 1905. 



DISTURBANCES OF NUTRITION 



lg 



caries, could be found. lie stated that in those teeth having livh 
pulps transparency might he found. 

Tumors. — A tumor is a new growth conforming to a degree to the 
normal histology of a part, but having no physiological function 
and no typical limit of growth. They are classed as benign or malig- 
nant, accordingly as they are strictly localized and comparatively 
harmless, or tend to sap vitality and to spread dangerously, or to be 
transferred to other localities (metastasis). 



Fig. 34 




Portion of a wall of an ovarian dermoid cyst: a, wall of the cyst; b, projecting portion 
made up of fatty and cutaneous tissue; c, hairs; d, teeth. (Ziegler.) 



The growth of a tumor is attended by a sapping of the vitality of 
a sufferer — the degree of the debility produced being apparently in 
direct ratio to the size and the rapidity of the growth. Besides the 
size and the rapidity of development of individual tumors, another 
element determines their malignancy, their position, and, further- 
more, their occurrence in other parts resulting in multiple tumor 
formation. A tumor victim acquires a peculiar appearance — a cach- 
exia whose intensity and rapidity of advance are directly dependent 
upon the degree of malignancy, and the effects produced upon 
general nutrition by the toxic substances entering the circulation. 

Tumors introduce no new form of tissue element; they are repro- 
ductions of the cells of the tissues of the body. They may have the 
same cell formation as the tissue from which they spring, and are 



TUMORS 73 

then called homologous tumors; or they may have a different histo- 
logical structure from the tissue in which they are found, being then 
called heterologous tumors. For example, a bony tumor growing 
from hone would be homologous; a cartilaginous tumor growing 
from gland tissue would be heterologous. 

Etiology. — The causes of tumor formation are unknown ; it has been 
believed that their growth is due to parasites, especially the protozoa; 
this, however, has not been proved. A certain proportion of tumor 
formations, 7 to 14 per cent., 1 appear to be caused by traumatic 
injury; as, for example, in cases of mammary tumor, a history of a 
blow or fall may be at times obtained. 

Long-continued, sluggish inflammation appears to be causative 
of tumor formation in an unknown percentage of cases. A chronic 
irritation of certain portions of the body, such as the junction between 
the mucous and skin surfaces of the lip, the sides of the tongue, etc., 
is a frequent antecedent to their formation. Ziegler gives a reason- 
able explanation of the origin of certain epithelial tumors in organs 
which are undergoing atrophy; for example, in advanced age the 
connective tissue of the body is undergoing atrophy and there is 
relaxation of its strata; the epithelium of the surface (or of glands), 
still possessed of its power of reproduction, proliferates and invades 
the connective tissue, producing cancer. 

Cohnheim advanced the theory that embryonic remnants or 
"rests" are included in the tissues and in time reassert their pro- 
liferative powers. 

Tumor formation consists in the reproduction of the cells of one 
or more tissues, and in the growth thus formed bloodvessels are 
developed. Tumors do not contain nerves, though they may develop 
in nervous tissue. 

" The bloodvessels of tumors have comparatively fragile and poorly 
developed walls. In the malignant growths or rapidly developing 
tumors of any sort the vessels are mere spaces between the tumor 
cells, with little attempt at the development of firm walls." 2 

About the more slowly developing tumors a condensation of con- 
nective tissue occurs in many cases, forming a distinct limiting wall 
or capsule from which the tumor may be enucleated. 

The two great classes of tumors, those of mesoblastic and those 
of epiblastic and hypoblastic origin, may be subdivided into orders 
according to their histological peculiarities. 

1 Ziegler. 

2 Stengel, A Text-book of Pathology. 



74 



DISTURBANCES OF NUTRITION 



Classification of Tumors. 



TUMORS OF THE MESOBLASTIC TISSUES. 



Those usually benign : 

Bony tumor, or osteoma. 
Cartilaginous tumor, or chondroma.- 
Fibrous tumor, or fibroma. 
Fatty tumor, or lipoma. 
Mucous tumor, or myxoma. 
Tumor of lymphatic vessels, or lymphangioma. 
Tumor of bloodvessels, or hemangioma. 
Tumor of nerve fibers, or neuroma. 
Tumor composed of neuroglia, or glioma. 
Tumor composed of muscle fibers, or myoma. 
Those usually malignant: 

Tumors of connective tissues with rapid cell proliferation and 
little intracellular substance: 

Spindle-celled sarcoma. 

Round-celled sarcoma. 

Giant-celled sarcoma. 
Sarcomata i Angiosarcoma. 

Sarcomatous cylindroma. 

Melanosarcoma. 

Mixed sarcomata, as fibrosarcoma, etc. 



TUMORS OF THE EPITHELIAL AND ENDOTHELIAL TISSUES. 



Those usually benign: 

Papilla of skin or mucous membrane — papillomata. 
Tumors of epithelial glands — adenomata. 
Those malignant: 

"Epithelial growths atypically reproducing certain glandular 
or other structures and showing a manifest tendency to 
irregular extension." 1 

Epithelioma f Squamous. 

Consists of surface Cylindrical 

epithelium I (columnar) . 

Glandular carcinoma 

(histologically resembles racemose gland). 
Colloid cancer. 
Syncytioma malignum 

(carcinoma of placental site). 



Carcinomata 



Stengel, A Text-book of Pathology. 



TUMORS 75 

Tumors are rarely com posed of but one type of tissue; several 
types may be present, the tumor receiving its name from the tissue 
predominating. When the distinguishing feature of a tumor is two 
predominating tissues, the tumor is given a compound name; as, 
for example, when, in a sarcomatous growth, numerous large multi- 
nucleated cells characteristic of bone-marrow are found it is called a 
myelosarcoma. When fibrous and sarcomatous tissue are distin- 
guishing features the tumor is called a fibrosarcoma. 

Tumors are dangerous in several ways : The size of the tumor may 
cause pressure upon important structures. The rapidity of growth 
may sap the vitality of the individual. If the tumor degenerate or 
suppurate, it may produce hemorrhages, or the absorption of the 
poisonous products may produce toxemia with anemia, emaciation 
and weakness, and a train of malnutritional conditions due to 
intoxications (p. 100). The metastasis of portions of tumors as 
emboli reproduces the tumor in a new T locality. In the connective 
tissues the sarcomata are the malignant types and the sarcomatous 
element in a mixed tumor determines the malignancy, e. g., in fibro- 
sarcoma. In the epithelial tissues the carcinomata are the malignant 
tumors, and in mixed tumors determine the malignancy. 

Malignant tumors are often associated with disturbance of the 
general health from their inception. They tend to recur after abla- 
tion and either invade the adjoining tissues which may cause grave 
local disturbance or the morbific material they form enter the cir- 
culation or lymphatics and thus are transplanted to other localities 
(metastasis) . 

Since the malignancy of a tumor is due primarily to the size and 
the rapidity of its growth, it is clear why sarcomata are more 
malignant than fibromata, and why some forms of sarcomata are 
more malignant than others. To illustrate: 

Begin observation at the different stages of connective-tissue 
development, when connective-tissue cells have first divided, repro- 
duced; the tissue produced is at the indifferent stage, as seen in 
section of the embryonic jaw (Fig. 35). 

Mesoblastic cells at this early period are in an indifferent stage; 
some of the cells shown in the figure will form bloodvessels, others 
will become bone corpuscles, others will form fibrous and others 
muscular tissue. This structure has its analogue among tumors 
in a soft, fleshy, rapidly growing growth, called the round-celled 
saccoma. As cells expend their vital energy in three ways (nutritive, 
functional, and reproductive activity) the embryonic cells of such 
a growth may expend their energy in nutrition (growth), and will 
then grow out of the indifferent stage into a more mature form of 



r, 



DISTURBANCES OF NUTHITIOS 



connective tissue, the ultimate form of one type being a fiber; an 
embryonic round cell undergoing a series of form changes from a small 
round cell to a long fiber (Fig. 36). The growth may cease at any 
stage of this form change, the tumor composed of such cell forms 
receiving a corresponding name. The embryonic connective-tissue 

tumors, as stated, are called 
Fig. 35 sarcomas, the form of the 

cells composing them giving 
them a qualifying title. 

In Fig. 36 are represented 
the stages of development 
of a connective-tissue fiber 
from a round cell. If 
growth cease at stage 1, and 
the cell energy thereafter 
expend itself in reproduc- 
tion, a rapidly growing 
tumor composed of small 
round cells is formed — a 
small round-celled sarcoma, 
markedly malignant. If 
the cells expend a portion 
of energy in growth of cell size, a large-celled sarcoma is formed, 
less malignant than the former. If the cells expend a portion of 
their energy in forming intercellular substance, reproduction and 
malignancy are less active. So the spindle forms, 3 and 4, represent 
less rapid reproduction and lesser malignancy than 1 and 2, although 




Porcine embryo : ct, embryonic connective tissue 
of mesoblast. 2.5 cm. X 250. 



1 2 3 

® ® -<& 



Fig. 36 



the form 4, which should be of less rapid reproduction than 3, because 
of more mature organization, is frequently more malignant, because 
less intercellular substance is formed, as shown in Figs. 37 and 38, 
the energy represented in that process being used up in reproduction. 
The nearer the approach to the mature form (6, Fig. 36) the slower 
the growth of the tumor, which, when composed of tissue of this 
type, loses its fleshy (sarcomatous) appearance and becomes fibrous, 
and is hence called a fibroma. 

When a sarcoma begins its growth from bone, its histological 
character is frequently modified (Fig. 39). It contains large marrow 



rrMoiis 



77 



cells which have undergone incomplete reproduction, forming giant 
multinucleated cells; this is a common form of tumor emerging 
from the sockets of teeth. Some of the cells of a sarcomatous growth 



Fig. 37 



Fig. 38 




Small spindle-celled sarcoma (from 
a tumor of the leg). X 200. 




Large spindle-celled sarcoma. To the left 
the cells have been separated by teasing, so 
that their individual forms are apparent; to 
the right they are in their natural state of 
apposition, such as would be seen in a thin 
section of the tumor. (Virchow.) 



may go on to maturity, while others remain at some stage of their 
developmental career. Malignancy will be modified according to 
the amount of mature tissue formed. 



Fig. 39 



Fig. 40 




Myeloid epulis from lower jaw: a, 
multinucleated giant cells; b, oval cells. 
X 265. (Pepper.) 




Adenoma of the breast: a, group of 
glandular acini; b, fibrous stroma; c, 
cells broken away from their attach- 
ment. X 265. (Pepper.) 



Epithelial Tumors. — Growths arising from epiblastic or hypoblastic 
tissues may be benign or malignant. What are called the adenomata 
may be taken as the type of the benign epithelioma; that is, compara- 



DISTURBANCES OF NUTRITION 



Fig. 41 



tively benign. They present all of the characters of typical glandular 
tissue; numerous acini lined with epithelial cells and surrounded by 
connective tissue (Fig. 40). Tumors of this type may lose their 
comparative benignancy and become of the succeeding epithelial 
type. 

Carcinomata. — These are growths arising from preexisting epithe- 
lial tissue, which possess the characteristics of epithelium developing 
without limitations of a basement membrane. Beginning upon a 
skin, or mucous surface, or in a gland, the reproduced epithelial 
cells are not sharply marked off from the connective tissue by a 
limiting membrane, but, gaining entrance to the alveoli of connective 

tissue, they proliferate there, find 
their way in-to lymphatic vessels and 
lymphatic glands, and reproduce epi- 
thelial growths in such places of 
lodgment, so that a tumor having 
its origin in one part may give rise 
to tumors in other parts of the body 
—metastasis (Fig. 41). Carcimomata 
of the mouth are frequently due to 
chronic irritation, as from smoking or 
pipe-stems, jagged teeth. Bay 1 states 
that it is rare in European women while 
common in men; that women of Cey- 
lon and India excite it by betel-nut 
chewing. 

Like the connective-tissue tumors, 
types of carcinoma differ as to rapid- 
ity of growth in their original situation 
and in the degree of transference; 
these factors determine their malig- 
nancy. Tumors of the sarcoma group may also give rise to growths 
in other parts, the tumor cells being carried thence by lymph 
vessels or bloodvessels. 

After a period, tumors frequently suffer such interference with 
their nutrition that degeneration occurs in them. 

After removal, some varieties of tumors, both those which infiltrate 

surrounding tissues and those which are metastatic, show a tendency 

to recurrence; that is, removal does not effect a cure, and the tumor 

upon reappearance assumes another and a more malignant character. 

Epithelial tumors never become tumors of the connective-tissue 




Section through an aggregation 
of very young cancer cells, lodged 
like an embolus within a capillary 
of the liver. The parent growth 
was an adenocarcinoma of the 
stomach. Preparation stained with 
hematoxylin. X 300. (Ziegler.) 



1 Dental Cosmos, June, 1913. 



DEFICIENCY OF NUTRITION; UYPONUTRITION 7 ( .) 

typo; and, vice versa, connective-tissue tumors cannot become 
epithelial tumors. 
The distinction formed between epiblast and mesoblast in the 

embryo is maintained throughout life. Tumors show a great variety 
of histological characteristics, for which works on general pathology 
should be consulted. 

While the treatment of tumors is not a part of this book, it may 
be said that, unless the cause of a tumor can be located and its 
benign character determined, it is wise to view it as dangerous. 
They should be usually removed surgically unless inoperable. The 
x-rays, radium rays, or Finsen light rays, etc., are useful in some 
cases after operation or in inoperable cases. 

Cooley, of New York, has suggested a toxin for injection which 
inhibits sarcoma and at times cures. Its use after operation is held 
advisable. 1 

The writer has been urged to introduce material upon tumors 
of the jaws. This seems inadvisable, as space does not permit. A 
tumor is readily seen and should be viewed with suspicion. If not 
dental as described hereafter, it should be referred to a surgeon 
for further diagnosis. 

DEFICIENCY OF NUTRITION; HYPONUTRITION. 

If the quantity or quality of the blood delivered to a part be 
deficient, the nutrition of the cells of the part is impaired. First, 
atony, a lessened activity of the vital processes of the part, occurs. 
Cell chemistry is disordered, and waste products are either retained 
in or about the cells. 

The function of the cells is diminished: If secretory, its secretion 
is lessened; if muscular, the cell has a lessened contractility; the 
relations between nutrition and waste are disturbed; the part 
becomes physiologically wearied sooner than usual. 

Hypoplasia. — If the process cause interference with the develop- 
ment of an organ, so that it is much below normal in size, or 'the 
development of a part is arrested, whether from lack of nutrition 
or disturbance of developmental cells, the resulting condition is 
termed hypoplasia. 

If the parts fail entirely of development, the condition is called 
agenesia. 

Atrophy. — If the process of hyponutrition be marked, the waste 
in a previously normal part may exceed repair, and the part affected 

1 Clinton, Dental Cosmos, 1910, p. 316. 



80 



DISTURBANCES OF NUTRITION 



becomes diminished in size or atrophied (Fig. 42, 7^). Atrophy may 
be general or local. In general atrophy there is a general loss of 
tissue, due to an excessive waste or faulty assimilation of food by 
the tissues. There is a loss of body weight, due first to a loss of the 
fat, later to shrinkage in the tissue cells. The shrinkage in size of 
the tissue cells causes shrinkage of the entire organ. The cells and 
fat may recover their size when the faulty waste or assimilation is 
corrected. During atrophy many cells are lost through the process 
of fatty degeneration and removed by the phagocytes (leukocytes), 
so that atrophy may, like hypertrophy, be both simple and numeri- 
cal. An atrophied part is pale and shrunken, contains less fluid, 
and is tough and fibrous. At times the fibrous portion or connec- 
tive tissue may increase as the cells diminish (scterosis). 

Causes. — General atrophy is caused: 1 (1) By a deficient supply 
of food material delivered to the tissue cells. This may be due to a 
primary food deficiency or any interference with its preparation for 
absorption or with its proper absorption or circulation. (2) By 
-excessive waste of the tissues generally, as in fevers, prolonged 
suppuration, etc. (3) By impaired vital activity of the cells them- 
selves, as in senile conditions. 

Fig. 42 




Adipose tissue: A, normal; B, atrophic, from a case of phthisis; a, single fat cell, 
with cell wall, nucleus, and drop of fat. X 300. (Virchow.) 

Local atrophy may be caused: (1) By a lessened circulation in 
a part due to obstruction of the arteries, veins, or capillaries, as, 
for example, by pressure. (2) By diminished functional activity or 
disuse of a part, as in the case of unused muscles or even bones. 
Certain organs are atrophied or resorbed as a part of the cycle of 
life, e. g., the umbilical cord, the roots of deciduous teeth, the thymus 
gland, the mammary glands after the menopause. (3) The loss of 
nervous connection of a part with the nerve centres controlling it 
(trophoneurosis), or through interference with nervous centres 



Green, 



DEGENERATION 



- 



having trophic 



influence upon a part. (4) Excessive functional 
activity may cause atrophy by producing a degenerative condition 
due to overstimulation. 

Degeneration. — If cells have reached the limit of their life cycle 
or have been subjected to influences markedly disturbing their 
nutrition, the proteids of which they are composed are replaced 
by new substances of somewhat obscure origin, which appear 
in the parenchymatous cells and connective tissue, markedly 
altering the histology and pro- 



Fig. 43 






ducing a pathological anatomy 
peculiar to each form of degen- 
eration. If the change is due to 
chemical changes within the tis- 
sues, it is a true degeneration. 
If the new substance enters the 
cell, it is an infiltration. 
~Tatty Infiltration. — In this 
condition the fat is found in 
globules in the cells, which 
globules tend to coalesce. The 
nucleus may be pushed aside. 
It is regarded as simply the 
storing of fat in healthy cells, 
though possibly an infiltration 
may occur in a debilitated or 
degenerated cell (Fig. 44). 
— Fatty Degeneration. — Fatty 
degeneration is a condition in 
which the pathological accumu- 
lation of fat is found in the 
substance of cells. The cell 
appears granular and fat-drop- 
lets appear within the substance of the protoplasm and give a black 
reaction with 1 per cent, osmic acid. These do not tend to coalesce, 
as in the case of fat infiltration. "The larger the amount of cell 
albumin replaced by fat the nearer is the whole cell to death" 1 (Figs. 
45 and 46). 

Three theories are held as to the origin of the fat : 

1. That the proteid of the cell is changed to fat. 

2. That fat is a normal part of cell proteid and simply becomes 
more visible because set free through the action of poison (such as 




Muscle fibers in simple atrophy. 
(Schmaus.) 



Green, Pathology and Morbid Anatomy 



82 



DISTURBANCES OF NUTRITION 



bacterial ferments or phosphorus) acting upon the combinaton of 
fat proteids in the cell. The administration of phosphorus to 
animals produces it. 

3. That the fat is infiltrated from the blood, as in fatty infiltra- 
tion, but into diseased cells. Thus animals were poisoned with 
phosphorus and then fed with fat foreign to the animals; the 
foreign fat was found in the degenerated cells. 



Fig. 44 



Fig. 45 




Liver cells in various stages of 
fatty accumulation. X 300. 
(Rindfleisch.) 



Ill 



1 m 






Fatty degeneration of cells: a, from a 
cancer; b, from the brain in chronic soften- 
ing. X 200. (Green.) 



Fig. 46 







&k\ 






Fatty degeneration of the heart, from a case of pernicious anemia. The protoplasm 
is replaced by globules of various sizes stained black by osmic acid.- The outlines of 
the fibers are irregular, owing to inequality in their distention. X 400. (Green.) 



Causes. — Depression of vitality is always the proximate cause, 
and as primary causes producing this depression may be mentioned : 

Tissue starvation from any cause, as from an altered food supply. 
The lack of oxygen in acute hemorrhage (suboxidation). The intro- 
duction into the blood of toxic substances, such as mineral poisons, 



CLOUDY SWELLING 



83 



c. </., arsenic, mercury, or phosphorus; chemical compounds, as 
carbon monoxid; leukomains, as in diabetes and chronic anemia; 
toxins, as in fever of bacterial origin or from a focus of infection. 
Locally, interference with the circulation, if not sufficiently over- 
whelming to produce death, may cause fatty degeneration of cells 
by interfering with the food supply, as in venous hyperemia, aseptic 
infarcts, and simple inflammation. The products of infection can 
produce fatty degeneration in the cells of the inflamed area. (See 
Pathology of Inflammation.) 



Fig. 47 



H>- 







Cloudy swelling of kidney epithelium: a, normal epithelium; b, epithelium begin- 
ning to be cloudy; c, advanced degeneration; d, cast-off degenerated epithelial cells. 
From a preparation which had been treated with ammonium chromate. X 600. 
(Ziegler.) 



In areas which have undergone fatty degeneration a cheesy sub- 
stance may be formed out of the degenerated elements existing 
in the part. The fluid is gradually absorbed and a mass composed 
of atrophied cells, fatty debris, and cholesterin crystals is left. This 
process is known as caseation. Encapsulation of the caseous mass 
by fibrous tissue may take place, or its liquefaction or its calcifica- 
tion may occur. Fatty degeneration may occur in many tissues, and 
the danger is proportionate to the importance of the tissue involved. 

Cloudy Swelling (Parenchymatous or Granular Degeneration). — 
Cloudy swelling is a change occurring in the parenchyma (essential 



84 DISTURBANCES OF NUTRITION 

cells) of a part as the result of the presence of toxic substances in 
the blood, or even as the result of aseptic disturbance of nutrition, 
such as a severe burn. The same causes which produce fatty 
degeneration may produce it. 

Pathology. — The cell absorbs fluid, swells, its contents become 
granular, and the histological structure is lost. In the early stages 
the change is albuminous; no fat is demonstrable; later, however, 
it appears, so that the change is regarded as a first stage in the pro- 
duction of fatty degeneration, by which process many of the cells 
are lost, though the organ may recover if the patient withstands 
the original disease (Fig. 47). 

Glycogenic Infiltration. — Normally, glycogen is found in some other 
tissues than those of the liver, notably in muscle. If it appear in 
tissue not normally containing it, or in excess in those in which it 
is normal, a glycogenic degeneration or infiltration exists. It may 
be produced by any influence which alters the behavior of cells, 
especially those having secreting activity toward the carbohydrate 
food element (glucose), as in diabetes, and, while mostly within the 
cells, may exist in the intracellular tissue. (Stengel.) It is stained 
brown by iodin and converted by ptyalin or amylopsin into sugar, 
the color reaction then not occurring. 

It does not seem to be clearly shown as a direct infiltration of 
glycogen, but rather as an appearance of glycogen in the cells, which 
may readily be glucose changed to glycogen within the cells. It 
has not been satisfactorily shown to be a degeneration from proteid 
constituents. (Stengel.) 

Cook 1 calls attention to the fact that the tissues become capable 
of diverted action, and that the glycogen may, even experimentally, 
be so acted upon by oxidizing agents as to be converted into acid 
derivatives, probably lactic acid, paralactic acid, and sarcolactic 
acid, and that these may be broken up by the zymotic action of 
tissue cells or by certain bacteria. The degenerative change in the 
tissues renders them susceptible to bacterial action, as in case of 
the gum tissue. 

The mucous membrane of the gums has been shown by the same 
author to be capable of this degeneration if overstimulated by chem- 
ical agents followed by the use of a stiff brush, and he argues that 
acid derivatives may be liberated either by the tissue or by bacteria 
in contact with them, and thus possibly account for certain phases 
of tooth destruction, as erosion. He emphasizes the fact that infil- 
tration of tissue, with abnormal quantities of a normal constituent 

1 Dental Cosmos, 1907. 



DEGENERATION 85 

of the body, is more likely to take place in the lymphoid and mucous 
cells of the body than in any other tissue structure. 

Hyaline Degeneration. In various forms of arthritis, in arterio- 
sclerosis, during- infection, in septic- processes, and in other condi- 
tions a retrogressive process, characterized by the appearance of a 
homogeneous proteid substance, occurs. It is closely allied to amyl- 
oid, mucoid, and colloid degeneration, and to coagulation necrosis. 
The new tissue is of a glistening, waxy, homogeneous appearance, 
and stains with great affinity with acid anilin stains, as acid fuchsin, 
taking a brilliant red color. The cells of the part may show fatty 
degeneration. 

Location. — Seats of interest are the -endothelium of bloodvessels, 
which is proliferated, making the wall thickened, and the lumen nar- 
rowed or obliterated. (See 

Endarteritis Obliterans.) ^ FlG - 4S 

Upon mucous membranes it 
causes opaque plates or 
pseudomembranes. It oc- 
curs in interstitial tissues 
and also within the cells. 
Its proximate etiology and 
pathology are obscure. 

The hyalin material can 
be reconverted, absorbed, 

' Hyaiin degeneration of small vessels in the 

and removed. It does not cord, x 350. 

injure the cells to an extreme 

degree. It may be converted into other albuminoid degenerations, 

may undergo caseation and calcareous infiltration. (Stengel.) It 

has been found in the epithelium of the mouth by Cook, but 

without established significance. 

Mucoid Degeneration.— In this form of degeneration the proteid 
protoplasm of cells is transformed into mucin, a glycoproteid charac- 
terized by affinity for basic anilin stains, as methylene blue. It 
occurs in catarrhal mucous membranes, connective tissue, tumors, etc. 
Mucin absorbs water, but is not soluble in it or dialyzable. In the 
catarrhal mucous membranes the goblet cells show excess in number, 
and are swollen and distended with mucin. (Stengel.) The cell 
becomes vacuolated and the nucleus granulates and stains with a 
basic stain. About the necks of teeth the mucus becomes stringy and 
tenacious, its chemical and physical character being changed and 
chondroitin present. (Cook.) 1 

1 Dental Cosmos, 1907. 




86 



DISTURBANCES OF NUTRITION 



According to this author this substance combining with water 
might give rise to sulphuric acid in contact with the teeth. Ci 8 H 2 7 
NSOi7+H20 = H2S0 4 +C 18 H27NOi4. Mucic acid might be produced 
from glycuronic acid found in mucin. Cook observed mucoid degen- 
eration of epithelial cells and submucous structure in cases in which 
strong astringents were used on the mucous membrane; the con- 
traction of the cells caused a retention of mucin leading to a chemical 
change in the mucin itself. (See Erosion.) 



Fig 




Colloid cancer, showing the large alveoli, within which is contained the gelatinous 
colloid material. X 300. (Rindfleisch.) 



Colloid Degeneration. — This consists of the abnormal appearance 
of a non-dialyzable substance like mucin, but differing from it in 
preference for acid stains, by not being precipitated by acetic acid 
and alcohol, by lack of absorption of water, also by causing a more 
profound disturbance of cells in which this is found and in which 
it remains much longer. Salts, as calcium oxalate, are apt to be 
precipitated in it, and may be again dissociated. The etiology is 
obscure, but probably analogous to that of mucoid degeneration. 

Dropsical Infiltration. — This is an infiltration of an excess of 
plasma into cells. It is a part of cloudy swelling, or may occur as 
large droplets of plasma enlarging the cell compressing the nucleus 
and protoplasm, and may even cause the cell to burst. Fatty degen- 
eration of the protoplasm may occur as a sequence to dropsical 
infiltration. The process occurs in general dropsy, in burns, in skin 
lesions connected with vesiculation, and in inflammation of organs. 

Lardaceous Degeneration. — This type of degeneration is known as 
amyloid, albuminous, or waxy. The formation of the material from 
which this condition derives its name is preceded by an unknown 



CALCAREOUS INFILTRATION 



87 



type' of degeneration of the cells of the part affected. The degenera- 
tive processes appear to be the result of long-continued suppuration 
due usually to tuberculous disease. In the connective tissue about 
the degenerated cells (not in the cells) a substance akin to albumin 
is deposited, which causes swelling and a pseudohypertrophy of the 
organ affected. The substance gives a reaction with iodin resem- 
bling that of starch; hence the name amyloid (amylum, starch). It 
may affect any organ of the body. It usually appears first in the 
connective tissue lying between the inner and middle coats of small 
arteries. The swelling caused by the infiltration markedly lessens 
the caliber of the vessels and diminishes the nutritive supply of the 
parts supplied by the artery, which may lead to fatty degeneration 
and atrophy of the insufficiently nourished parts. 

Fig. 50 




Calcareous infiltration of renal epithelia. From the edge of an old infarct; a few 
tubules still to be recognized. X 250. (Schmaus and Ewing.) 

Calcareous Infiltration. — In tissues which have undergone pre- 
vious degeneration, calcium, sodium, or magnesium salts may be 
deposited as an infiltration from the blood plasma. The parts are 
thus petrified. The cells take no active part in the process. 1 

It is believed, however, that the deposit of salts in the dying tissue 
is «more than a mere precipitation, and that calcification results from 
a combination of the salts with an albuminous base and with fatty 



Green, Pathology and Morbid Anatomy. 



88 DISTURBANCES OF NUTRITION 

acids, such an affinity being favored by the degenerative changes. 
Ordinarily, the carbonate and phosphate of calcium are the infiltra- 
ting salts, but in gout uric acid salts are deposited, owing to an excess 
of uric acid in the form of biurates and quadurates in the body fluids. 
A sluggish circulation in the part favors the deposition of the salts. 
The calcification may occur in both the cells and in the intercellular 
substance. 1 (See Calcific Degeneration of the Pulp.) In the early 
stages the salts are found as fine granules in the intercellular substance. 

"The white, fibrous tissue is the form of connective tissue usually 
affected, but concretions may occur in the connective tissue sur- 
rounding the bloodvessels." 2 

As a secondary process after degeneration, calcification of the 
middle coats of the arteries may occur, rendering them inelastic. 
This renders them incapable of regulating the blood supply to parts, 
and these suffer more or less nutritive disturbance, and, in some cases, 
actual death of the part (gangrene). Calculi are found in tumors at 
times. Many forms of free calculi are formed in the body. These 
occur most frequently in ducts or cavities lined with epithelium, 
e. g., the salivary ducts and the bladder. 

"All free concretions have an organic basis or nucleus," with 
which are combined the calcium salts, oxalates, cholesterin, etc., 
making up the inorganic or crystallizable part of the combination. 
The organic part may consist of inspissated feces, as in enteroliths, 
mucus, or mucin, as in the calculi upon the teeth; epithelial scales, 
mucus, etc., in the urinary passages. 3 The fine crystals or granules 
are probably soluble in some cases. The larger calculi are probably 
permanent and cause degeneration of adjacent tissue. 

Calcareous infiltration is clearly to be distinguished from the 
normal calcification of the hard tissues, bone, enamel, dentin, and 
cementum. These are composed of calcoglobulin, in which calcium 
and magnesium salts are combined under the superintendence of 
certain living cells with albuminous bases derived probably from 
their own substance. 

Pigmentary Infiltration (see Tooth Development). — Pigmentary 
infiltration is the infiltration of coloring matter into the tissues. 
There are four varieties: 

1. Extrinsic, derived from outside the body, e. g., coal dust 
in lung tissue or general staining from silver salts taken up in the 
intestines. 

2. Hematogenous, derived from hemoglobin or its derivatives. 
They are: 

1 Ziegler, General Pathology. 2 Ibid. 3 Ibid. 



NECROSIS 89 

(a) Hemoglobin, dark red, 
{b) Hemin, reddish brown or bluish black. 
(c) Methemoglobin, brownish red. 
(//) Hematin, dark brown or bluish black. 
(e) Hematoidin, orange or reddish brown. 
(/) Hemosiderin, yellowish or brownish. 
These are decomposition products of hemoglobin. Hemoglobin 
and hemosiderin contain iron. 

3. Hepatogenous, or biliary. 

4. Metabolic, resulting from cellular activity w 7 ithin the body, 
and termed melanin. 

The hematogenous pigments are of chief interest, inasmuch as 
they occur in the staining of teeth by devitalized pulps and sometimes 
by living pulps in a state of venous hyperemia. In these discolora- 
tions there is an analogy to the colors manifested in an old bruise, 
which undergo various color changes as the chemical character of 
the pigment is altered. (See Moist Gangrene of the Pulp.) 



NECROSIS. 

Necrosis (from nekros, dead) signifies, in its broadest sense, death 
of tissue. It is due to profound disturbance of its nutritional func- 
tion or to direct injury to its elements. 

Necrosis proper (per se) signifies death of tissue in mass from any 
cause. 

Necrobiosis means the death of cells through the process of 
atrophy or degeneration, which are successive changes leading to 
death. 

Necrosis of bone signifies the circumvallation and death of bone 
through the process of inflammation, which causes thrombosis of 
its vessels and cessation of its nutrition. The dead part, when 
separated, is called a sequestrum. The solution of continuity is 
effected by leukocytes massed about the portion in which nutrition 
has ceased. 

Caries of bone is that form of bone death in which the bone is 
honeycombed and molecularly broken down rather than seques- 
trated. (See Osteoporosis.) 

Gangrene is a term used to signify death, en masse, of a part, 
the soft parts being included. The dead part undergoes drying 
(dry gangrene) or putrefactive softening (moist gangrene). (See 
Gangrene.) 

Etiology. — The causes of necrosis are as follows : 



90 DISTURBANCES OF NUTRITION 

1. Circulatory obstructions, as (a) stoppage of an artery supplying 
a part, the nutritive supply being cut oft' by any cause; (b) venous 
hyperemia of a part, the vein being unable to carry oft' the blood 
charged with cellular waste, which accumulates about the cells, 
intoxicates them, and prevents access of fresh blood (food supply) ; 
(c) occlusion of the capillaries by any cause has a similar effect. 
Inflammation may be placed in this general class of causes. 

2. Trophic Disturbances. — The nerves controlling the metabolism 
of a part being diseased, the part undergoes degeneration and slight 
causes produce necrosis, e. g., necrosis of eyeball when excision of 
the Gasserian ganglion has been practised. 

3. Direct destruction of the vital activities of cells by any physical 
or mechanical agents, or chemical substances, including among the 
latter the poisonous substances produced through the action of 
bacteria. (See Fig. 77.) 

Injuries, blows, the tension of exudate, pressure, excessive heat 
or cold, the passage of powerful electric currents, and the ar-rays 
are all influences which directly injure or permanently destroy vital 
activities of cells. The application of chemical agents which so act 
upon cell substance as to change its character produces necrosis. 

While this is particularly true of such substances as powerful 
acids and alkalies, or alkaloids, w T hich immediately destroy cell 
integrity, it is also true of milder agents acting for longer periods. 
Certain poisons, particularly those of bacterial origin, paralyze the 
vital activities of cells, and necrosis results. 

The occurrence or non-occurrence of or the liability to necrosis 
will largely depend upon the degree of vital energy of cells prior to 
the action of the active causes of necrosis. Parts debilitated from 
any cause are more liable to necrosis than those which have suffered 
no debility. A part chronically ill-nourished, subjected to the causes 
producing degenerations, is liable to suffer necrotic changes, for the 
several degenerations and atrophy are but successive stages leading 
to necrosis. 

A necrosed part acts as an irritant to the tissues about it, inaugu- 
rating an inflammatory reaction which marks off the dead from 
the living parts. The dead part is sequestered, and hence is called 
a sequestrum, or, in case of soft parts, a ''slough," or sphacelus. 

Necrosis may be of several types, of which the following are the 
chief forms: 

Coagulation Necrosis. — When a dying tissue contains coagulable 
material and the necessary ferments, the parts undergo coagulation. 
(See Coagulation.) The cells and parts about become solidified, the 
cells lose their nuclei and do not stain as usual, and the part appears 






GANGRENE 91 

glazed, pale, and waxy. It occurs in suppuration, and is due to the 
coagulating ferments of pyogenic cocci. (Sec Bacterial Ferments; 
also Fig. 63.) 

The thrombosis of the vessels about an area of infective inflam- 
mation is probably due to the same ferments. 

Fat Necrosis. — This is a peculiar form of fat death in which the fat 
is split into glycerin and fatty acid by lipase (a ferment). The fatty 
acid remains and combines with inorganic salts. 

Liquefaction Necrosis. — This is the death of tissue with liquefaction 
of the proteid material in the area, which is usually rich in exudates. 
The process is probably due to enzymes capable of liquefying the 
tissue. 

GANGRENE. 

When death, en masse, of a part occurs as the result of an inter- 
ference with its nutritive supply, the process is termed gangrene, 
regardless of the subsequent results in the dead tissue. 

Causes. — It may occur as the result of an inflammation produced 
by a particular bacterium, as in noma or malignant edema; from 
arterial obstruction, as arterial thrombosis; or capillary obstruction, 
as in freezing or venous obstruction, may produce it. (See Venous 
Hyperemia of the Pulp.) Ergot may produce it through contraction 
of the bloodvessels. 

Dry Gangrene. — In parts which ordinarily contain but little 
fluid the obstruction of the artery may be associated with but little 
obstruction of the veins and lymphatics. Under such circumstances 
the dead part is drained of the little fluid it contains, and a fresh 
access of fluid is prevented. Exposure to the air aids a further loss 
of moisture by evaporation. The conditions are not favorable to 
the development of microorganisms, and the part changes from pale 
appearance to a dark, shrunken one. The process of gradual drying 
is also called mummification. (See Dry Gangrene of the Pulp.) It 
is usually circumscribed. 

Moist Gangrene.— Under opposite conditions — i. e., a venous 
obstruction with a fair arterial supply — there is much venous 
engorgement and extravasation of blood into the tissues, which are 
stained red by the hemoglobin from disintegrated red corpuscles. 
Abundant effusions also cause the part to be swollen. Death of 
tissue occurs from interference with nutrition; when bacteria are the 
direct cause, the part is inflamed and edematous. The moisture 
present favors the development of bacteria, and they enter the tissue 
through the skin. Putrefaction with the evolution of malodorous 
gases, such as hydrogen sulphid (H 2 S), hydrogen phosphid (HP 3 ), 



92 DISTURBANCES OF NUTRITION 

and ammonium sulphid (NHOA causes the part to have an offensive 
odor. 

U the gangrene be due to infective inflammation, or the surrounding 
tissue be debilitated from any cause, the area of gangrene may spread 
— i. c, invade the living tissue (spreading gangrene). This is prob- 
ably due to the presence of bacteria, which irritate and progressively 
destroy the surrounding tissue. The poisons produced, if absorbed, 
may cause death. If the adjacent tissue be healthy and resistant, 
a line of demarcation is established, consisting of leukocytes, which 
dissolve all fibers or firm connections between the dead and living 
parts. Suppuration occurs at the line, and the dead portion is 
separated as a sphacelus or slough. Occurring in bone, this is called 

Fig. 51 




Senile gangrene of the great toe, from a case of arterial thrombosis. The toe is 
shrunken and its epidermis is being exfoliated. At the line of demarcation the skin 
has retracted (a) and the deeper parts are separating (b). (Green.) 

a sequestrum. An ulcerated surface is left. The latter form is cir- 
cumscribed gangrene. If gangrene be deep-seated and septic, sup- 
puration occurs, which establishes one or more fistulse upon the 
surface of the body or in one of its cavities. (See Moist Gangrene 
of the Pulp.) A sequestrum may be cast out through one of these. 
Occasionally the part being internal is encysted and the contents 
may be absorbed and the sac calcified. 1 In the aged atheromatous 
or calcareous changes in the arteries produce a slow circulation in 
the extremities. A slight injury to a vessel wall may induce extensive 
thrombosis (which see). The result is gangrene of a part or all of 
an extremity, known as senile gangrene (Fig. 51). 

1 Stengel, A Text-book of Pathology. 



GENERAL MALNUTRITION 93 

GENERAL MALNUTRITION. 

By the term malnutrition is meant a more or less general dis- 
turbance of the metabolic processes of the cells of the body, which 
may simply lower the body resistance or health standard, or may be 
of such profound character as to incapacitate an individual for 
ordinary functions. 

According to Howell, 1 some fourteen amino-acids and four di- 
ami no-basic bodies represent the construction of the proteids of the 
body which individually may contain all or a portion of the list. 
These amino-acids and polypeptids, making up the proteid-making 
food material in the blood, are thought to be derived by synthesis 
in the intestinal wall or liver of the elements derived from proteid 
food taken at the mouth through gastric (peptic) and pancreatic 
digestion in the alimentary canal, which are said to be completely 
hydrolized therein. When these amino-acids and polypeptids 
present at the cell the cell enzymes construct such as they require 
into cell proteid. Carbohydrate materials, fats and salts and oxygen, 
are also utilized by the cells. In cell catabolism the specific chemical 
substances which are the waste products of the special protoplasm 
of particular cells, probably go to other organs, as the liver, and 
are there changed. The ammonia salts are changed to urea, which 
is the most constant and bland of nitrogen excretions. The mono- 
amino-acids and diamino bases are also changed to urea. Uric acid 
is also in part changed into urea, and even food (as simple amino- 
acids) may be formed into urea without entrance into tissue 
formation. 

The purin bodies have a common purin nucleus or basis which 
with one atom of oxygen added forms hypoxanthin, two atoms of 
oxygen added form xanthin, three atoms form uric acid, which, as 
stated above, may be changed into urea. Adenin and guanin, two 
other purin bodies, are considered to be hydrolized by adenase and 
guanase or deaminizing enzymes into hypozanthin and Xanthin 
respectively; these again are oxidized by another enzyme (zanthin 
oxidase) into xanthin and then into uric acid. 

Some purin bodies come directly from food (also urea, see above), 
but also in part are formed in the body. 

The catabolism of sugar in the body is uncertain, it being thought 
that enzymes produce intermediate products which oxidases change 
to carbon dioxid and water and that the internal secretion of the 
pancreas is in some way essential. The fats are supposed to be 

1 Toxt-book of Physiology. 



94 DISTURBANCES OF NUTRITION 

changed into fatty acids and glycerin under the influence of lipase, 
controlled by the liver through an unknown series of changes. 

If imperfect digestion, assimilation, or elaboration of food materials 
or its circulation, or an imperfect relation between the amount of 
oxygen and food material at the cell exist, or if a great excess of food 
material be assimilated which cells cannot appropriate, and the 
excess acts as material to be gotten rid of, or if the food taken be 
of an irritating nature, or if such material as retained body waste 
products, toxins derived from foci of infection, or from alimentary 
canal, or drugs absorbed are presented to the cells in excess, or if 
the drain upon the body cells reduce the amount of cell protoplasm, 
and the replacement of the cell constituents is not rapid enough 
to restore the protoplasm wasted in energy, it is plain that a general 
disturbance of body cells may result, and the altered metabolism 
in turn furnishes its share of irritating, unfinished catabolic products 
to further increase the general disturbance through the production 
of a pathological condition of the blood (a humoral condition, 
Michaels). The gradual action of one or other of these classes of 
causes, acting either by starving the cells or by irritating them 
(auto-intoxication), produces a condition with tendency to diseases 
of certain type, and the tendency is called diathesis (acquired). 

According to Michaels, 1 following Gautrelet, the abnormal vital 
processes tend in mankind to pathological conditions, which we 
may classify under two humoral conditions (or diatheses), viz., 
hypoacidity and hyperacidity. The first state ("lymphatism") is 
the expression of a vital overactivity, and has, as consequences, the 
contagious diatheses (scrofula, tuberculosis, syphilis) . The oxidations 
are overactive, and the hydrations are superior to the normal; hence 
there is a decrease in organic acidity and an increase of saline 
chlorides excreted by the economy. Hypoacidity favors chemical 
changes in the tissues. (Ducleaux.) In the hypoacid diathesis all 
the oxidations are exaggerated, and are above the normal. 

"In the hyperacid diathesis (arthritism), gout, rheumatism, 
sclerosis, oxidation is insufficient; there is incomplete oxidation 
with a consequent increase of organic acidity or hyperacidity, and 
a peculiar state of the organism characterized in a general way by 
a slowness in the biochemical changes. The reaction of the blood 
with the ordinary reagents (litmus, for example) is normally alka- 
line, 2 but if we study the distribution of the acids and bases of the 
blood plasma we see that the reaction is really acid (Gautrelet, 
Drouin, and Hugeounenq), and thus acidity is increased and the blood 

1 Sialosemeiology, Proceedings Third International Dental Congress, 1900. 

2 Neutral to Phenolphthalein (Howell). 



GENERAL MALNUTRITION 95 

may become relatively acid by the accumulation of acid waste 
products which are not eliminated, the secretions and excretions 
becoming then of acid reaction. It is on this account that a certain 
number of chronic diseases have constant characteristics in regard 
to semeiology; increase of the normal acidity of the urine, as well 
as the increase in the normal acidity of the saliva." Following 
Gautrelet, he gives four effects of the exaggerated and retrograde 
processes that diathesis produces: (1) a chemical modification of 
the plasma; (2) modifications affecting the chemistry of secretions 
and excretions (as detailed above); (3) histological modifications in 
the tissues; (4) modifications due to the creation of a special field 
for microorganisms. It will be seen that the above effect begins 
with a change in the blood or its contents, which successively acts 
upon glandular and other cell physiology and later alters their 
histology, and in total may bring about a predisposition to bacterial 
invasion through the loss of vital potential or resistance. The 
hyperacid diathesis may be inherited or acquired by individuals 
who take a liberal supply of food requiring oxidation and take 
insufficient exercise in the open air, while in the hypoacid the 
oxidation is superior to normal. 

These diatheses are the forerunners of many of the diseases of 
malnutrition, and evidence of approaching disease may be obtained 
from both saliva and urine by analysis of their contents through 
physical, chemical, and micropolariscopic examination of either or 
both fluids. The contents of each fluid being taken out of the 
blood through glandular activity represent fairly the faulty elements. 
The presence of altered physical characteristics when fresh or upon 
standing, of unusual chemical substances determinable either by the 
aid of reagents or microscopic or micropolariscopic examination, 
leads to the inference that unusual chemical changes have oc- 
curred in the cells, or that the waste products found represent 
an undue waste of tissue, or that cell waste has been altered after 
leaving cells or not sufficiently changed into the normal waste 
products. 

In the accentuated disease condition one or more organs, as the 
liver and kidney, may be diseased, and it may be a nice point to 
determine whether the disease begins with the liver and proceeds 
to the diathesis, or with the diathetic condition or its cause and 
proceeds to disturb the liver. At the same time the same course 
might act upon both; for example, overfeeding with food requiring 
oxidation, and this not supplied by exercise, could induce a disturb- 
ance of the function of liver cells quite as readily as of any other 
bodv cells. 



96 DISTURBANCES OF NUTRITION 

According to Kirk, 1 the disproportion between pabulum and oxygen 
resulting in hyperacidosis produces a greater ratio of carbon dioxid 
to oxygen in the blood than is normal. Temporarily this would be 
corrected by the action of the renal epithelium in which a reaction 
occurs between the carbonic acid of the blood and the basic phos- 
phates, as follows: HNa 2 Po4+H 2 Co3 = H 2 XaPo4+HNaCo3. The 
sodium bicarbonate formed is returned to the blood, maintaining its 
alkalinity, and the acid sodium phosphate is eliminated as the normal 
acid salt of the urine. In the same way acid calcium phosphate is 
formed. 

When the disproportion between pabulum and oxygen are con- 
tinued, the suboxidation becomes chronic, the kidney is no longer 
sufficient to maintain alkalescence of the blood by eliminating 
the excess of acidity as acid phosphate, the carbonic acid seeks 
other channels of elimination, and the epithelium of the buccal 
glands and sweat glands may take up the action normal to the 
kidney and excrete acid sodium phosphate and acid calcium phos- 
phate, producing in the case of the buccal glands a certain class of 
erosion of the teeth, and in the case of the sweat glands frequently 
giving rise to eczematous eruptions. Dental caries is not ordinarily 
introduced in this stage, but if begun the carious matter is changed 
to a dark brown color, crumbly, semihard texture, and the further 
process is one of decalcification rather than a true carious process. 

"The continued suboxidation and hyperacidosis by carbonic 
acid thus leads to the great loss of basic phosphates as acid phos- 
phates, which are more readily soluble and osmosed through kidney 
epithelium than basic phosphates, and for that reason are rapidly 
eliminated', thus establishing a phosphaturia, with consequent 
phosphatic starvation and ill health, as shown by neurasthenia, 
with its irritability, despondency, migraine, cerebral hyperemia, or 
hysterical phenomena. A point of depletion is reached and they 
are found only in minute quantity in the urine and saliva. At about 
this time lactates of sodium, calcium, and magnesium, in the order 
named, appear in the saliva, then double lactates of sodium and 
calcium, then lactophosphates of calcium and magnesium, then 
oxalate of sodium or double oxalate of sodium and calcium, while 
oxalate of magnesium may appear in the urine. With the appearance 
of the lactophosphate a general rather than a localized erosion 
appears. (See Erosion.) The nervous irritability is markedly 
increased, and a rapid loss of weight occurs. Later, acetone and 
diacetic acid appear in the secretion along with creatin, and in some 

1 Dental Review, 1903. 






GENERAL MALNUTRITION 97 

cases c\ stin, at which period profound mental torpor, at times 
almost amounting to coma, is not infrequently manifested, or there 
may be extreme nervous irritability amounting almost to hysterical 
mania. 

" Coincident with the loss of the phosphates, nitrogen with carbon 
as a cyanogen radial (ammonium cyanate), which probably should 
have gone to form urea, is lost. Evidences of imperfect oxidation 
of proteids are manifested in the saliva and urine by the presence of 
lactate of ammonia (a forerunner of urea), lactate of calcium, creatin, 
acetone, and oxalates, with increase of urate of ammonia and amor- 
phous urates. The urine often contains indican, especially in cases 
complicated with disordered liver and habitual constipation. The 
saliva is usually constantly acid, due to the presence of acid phos- 
phates, and the dental lesions are ordinarily erosion, or, where the 
acidity is absent, pyorrheal invasion of the peridental membranes. 
Many of these cases develop epithelioma or leukoplakia buccalis, 
or both together, and in view of the fact that there is constant irri- 
tation of epithelium by the exudates, they may have an etiological 
relation/' (Free quotation, Editor.) 

The diet indicated by Kirk for these cases would apply to those 
diseases and cases of pyorrhea in which the predisposition is due to 
this diathetic fault, and consists in reducing the necessity for oxygen 
by largely eliminating the carbohydrate portion of the diet. Suc- 
culent vegetables, gluten bread, milk, albumin, and a moderate 
ration of proteids in the shape of fish, oysters, game, light meat of 
fowls, are allowed. Small doses of phosphorus, or of arsenic iodid, 
and glycerophosphates of lime and soda are continuously adminis- 
tered. The exercise and rest are adjusted, and attention is given to 
general hygiene. 

"Michaels found the saliva of but few individuals to be in a 
perfectly normal condition and the teeth perfect, while most of 
them are out of equilibrium and the teeth are affected either by 
caries or erosion or pyorrhea alveolaris. He states that lesions of the 
liver and kidneys cause the appearance of acid waste, also that the 
organism constantly produces acids, such as uric, oxalic, lactic, 
volatile fatty acid, etc., which, under normal conditions, are also 
destroyed, but that abnormal conditions arise which retard the 
oxidations of these organic acids, which must then accumulate in 
the organism among the waste products arising from incomplete 
dissimilation; many have acid properties. 

"The serum of venous blood, while weakly alkaline, has a real 
acidity (acid elements) stronger than that of arterial blood. Fever 
is accompanied by an acidity of the blood, as in diabetes (/3-oxy- 
7 



98 DISTURBANCES OF NUTRITION 

butyric acid), rheumatism, arthritism (gout). The alkalinity is re- 
duced (real acidity increased) in anemia, leukemia, and all cachexias. 

"He regards the liver as determining the majority of nutritive 
changes, and that it suffers from the influence of all sorts of toxins, 
whether the result of microbic activity or due to an excess of alkaloids 
(leukomains). The cells of diathetic individuals constantly elabo- 
rate products, some of which are positively poisonous to the hepatic 
gland. The acid salts and biliary pigments are toxic. Their absorp- 
tion is deleterious and the inactivity of the hepatic cells creates a 
danger to the organism. The danger arises from the fact that the 
liver has to eliminate from the circulation all kinds of debris. If 
the neutralization of the products of fermentation is incomplete; 
if the harmful ammoniacal compounds have not been changed 
into urea; if the liver does not have a reserve of glycogen, or if its 
generators, which are supposed to play a role in the metamorphosis 
of alkaloids, if through its inactivity there is a retention of waste 
products, the secretions are necessarily contaminated with the morbid 
principles; the toxic products present in the blood poisons the 
organism and constitutes the different diatheses (auto-intoxication)." 

This conception includes the views of physiologists that the liver 
is both a secreting, excreting, and food-elaborating organ. He argues 
that if the bacterial fermentations, by their presence or by the pres- 
ence of their toxins, are capable of modifying the enzymic secretions, 
they necessarily influence the action of the physiological fermenta- 
tions. It follows from this that these toxic principles saturate, 
in a given period of time, the organic secretions and produce a 
cacochymic state (morbid state of the body fluids). 

Michaels has found in the saliva of hypoacid individuals glycogen, 
albumin, perhaps inosite, mucin, basic chlorids with ammonia in 
greater quantites than normally, sulphocyanids and biliary acid 
in less proportion than normally, and concludes that it is an ideal 
medium for the development of microbic contagion. He has found 
glycogen in the saliva of adolescents generally, and susceptible of 
reduction and fermentation under the influence of ptyalin in the 
presence of earthy salts, a fact emphasized by Kirk with a view to 
its establishment as a prominent factor in susceptibility to caries 
(which see). In the saliva of hyperacids he found sulphocyanids 
and mineral and organic acids, acid phosphates of sodium and potas- 
sium, ammoniacal oxalates, biliary elements, and urobilin in greater 
proportions than normally. 

The increased importance of the consideration of metabolic 
diseases in their relation to dental diseases by the dentist warrants 
the introduction of a brief summary. 



GENERAL MALNUTRITION 99 

Inanition. This is ultimately tissue starvation, whether due to 
any of the following causes: 

1. Want of proper amount of food. 

2. Gastrie diseases interfering with digestion by altering the 
quality or quantity of hydrochloric acid or pepsin. 

3. Disease of the liver, etc. 

4. Abnormal intestinal digestion. 

5. Occlusion of the sorbefacients by retained excrementitious 
matter or other local disease. 

Effects. — The tissues are not properly supplied with food to 
maintain themselves, and waste exceeds repair; the unimportant 
parts are first consumed and make good the deficiency. The surplus 
food materials, first the fats, are first consumed, then the carbo- 
hydrates, next the nitrogenous tissues, first muscles and glandular 
organs, and, lastly, the osseous and nervous tissues. 

This is general atrophy necessarily accompanied by degeneration. 
There is loss of energy and temperature, and the vital organs are 
weak; death occurs from exhaustion. 

Overfeeding. — The excessive use of proteids in food leads to a 
necessity for elimination from the blood of the excess absorbed, and 
to intestinal fermentation of the unabsorbed excess. The proteid 
food maintains the proteid equilibrium, and any more than is 
required for this is in excess. 

Energy is largely supplied by the carbohydrates (eventually 
glucose) and the fats. An excess of these leads to the storing of fat 
to a degree normal and useful as a reserve, but in combination with 
a sedentary mode of life, pathological fat or obesity, in which 
oxidation is reduced. A tendency to fat production exists in in- 
dividuals. The presence of food excess means an overstimulation 
of metabolism with possible alteration, which may lead to general 
disease of malnutritional type and predispose to infections, etc. 

Excessive Tissue Destruction. — The tissues may be excessively 
wasted by many causes, and in many cases the food supply is defi- 
cient as well. These causes are, briefly: 

1. Fevers. 

2. Continuous hemorrhage. 

3. Long-continued suppuration. 

4. Tumors, especially carcinoma. 

5. Chronic infectious diseases, as tuberculosis. . 

The increased waste is due either to increased oxidation of the 
proteid elements, due to stimulation of nervous centres controlling 
catabolism, or to the ferment contained in the toxic substances 
produced and entering the blood, which may cause cellular waste 



100 DISTURBANCES OF NUTRITION 

in the effort to produce antitoxins (see Ehrlich's Side-chain Theory), 
while at the same time normal food appropriation is interfered with 
if the amount of food supplied is not indeed lessened, as in continuous 
hemorrhages. 

Intoxications. — These may be divided into extrinsic and intrinsic; 
intoxications. The principal classes are: 

1. Intestinal Intoxications. — In intestinal putrefaction, particularly 
in constipation, the aromatic products, acetone, tyrosin, indol, 
skatol, phenol, cresol, and paracresol, may be absorbed and produce 
a form of intoxication of tissue cells which lowers the vital potential 
of all cells and the resistive force of tissues to bacterial infection. 
In intestinal putrefaction in children a marked readiness of the 
muscular system to fatigue has been noted, also in cases of persons 
who have suffered from indicanuria for a long time, showing a mark- 
edly poisonous effect upon muscle and probably upon other tissue. 

The absorption of indol and its modification in the liver lead 
to its appearance in the urine as indican, or indoxylsulphate of 
potassium/ which, therefore, indicates an abnormal intestinal putre- 
faction with absorption of deleterious products. 2 

That indican in the urine is caused by abnormal tissue metab- 
olism is not well supported by evidence. 3 

It is found in carcinoma and chronic peritonitis. It is generally 
present when suppurations are in progress; probably indol is ab- 
sorbed from the focus of putrefaction. The ingestion of pus from 
pyorrheal pockets in the mouth may easily lead and has led to chronic 
gastritis and intestinal putrefaction, in which latter Bacillus coli 
communis plays an important, assistant part. The liver may be 
disordered primarily, thus favoring the condition owing to lessened 
formation of bile, or, secondarily, owing to its increased function 
as a poison destroyer. The intestinal putrefaction causes the forma- 
tion of indol, etc., thus leading to the presence of indican in the 
urine. The excessive use of proteid food not only overloads the 
intestine, but invites putrefaction therein ; also, the amount absorbed 
being excessive, the eliminative functions are overtaxed, leading to 
disease. 

2. Drug Intoxication. — The use of arsenic, phosphorus, or other 
inorganic poisons, or the vegetable alkaloids, as morphin, cocain, 
atropin, etc., or the continued contact with lead salts, all un- 
doubtedly affect metabolism — some beneficially— when employed 

1 Thompson's Practical Medicine. 

2 Test for indican: Add nitric acid to urine — shake with chloroform — a bluish 
color is imparted to the chloroform on standing. 

3 Leathes, Problems in Animal Metabolism. 



GENERAL MALNUTRITION 101 

in suitable doses in diseased conditions, or injuriously in continued 
excessive use. Thus atropin in small doses checks secretion — e. (/., of 
the salivary and mammary glands. Phosphorus continued produces 
fatty degeneration. 

3. Bacterial Intoxication. — The toxic products of bacterial action 
(apart from the aromatic products), as the ptomains and albumoses 
(toxins), act as ferments upon proteid tissue, causing cellular waste 
either by ferment action (destruction) or by stimulation of the cells, 
either directly or through the nervous system, leads to the produc- 
tion of antitoxic substances in excess, which by Ehrlich are claimed 
to be discharged into the blood. No doubt the cell is also rendered 
less capable of anabolism. (See Side-chain Theory.) This is seen 
in fevers in which emaciation (excessive waste) is proved by the 
increased output of urea. 

4. Intrinsic Intoxication. — In this class may be placed all intoxica- 
tions produced by substances originating in excess within the body 
proper as a result of metabolic disturbance, resulting from disease of 
the nervous centres controlling metabolism or of organs which fail to 
perform their duty of elaboration for metabolism or elimination or 
elimination proper, in part or entirely. In some cases compensatory 
elimination by other organs occurs, which may be effectual or may 
lead to disease of said organ or organs. A good example of com- 
pensatory elimination is seen in health during sudden changes of 
atmospheric temperature. Thus on the warm days perspiration is 
free and elimination by the urine lessened; the avenue of elimination 
is largely reversed on the cold days. These intoxications may also 
be classed : 

Uremia. — In this there is a retention of urea (as ammonium 
carbonate or its congeners) in the system which should be eliminated 
in the urine. The body cells are chronically or acutely poisoned, 
according to the degree of the retention, death resulting in the 
complete form. Nephritis is a common cause. 

Diabetes Mellitus. — In this disease probably the essential lesion 
is a hyalin degeneration of the islands of Langerhans, of the pan- 
creas, or injury to the floor of the fourth ventricle of the brain 
(diabetic centre), which may be caused by even strong mental 
emotion, as grief. 

Carbohydrate assimilation is interfered with: an increased amount 
of sugar appears in the blood (hyperglycemia) and urine (glyco- 
suria), and the cells are unable to appropriate it. Protein destruction 
with increased production of urea occurs (excessive waste). 1 An 

1 Stengel, A Text-book of Pathology. 



102 DISTURBANCES OF NUTRITION 

excess of phosphoric and sulphuric acids, jS-oxybutyric and diacetic 
acids arc formed or retained, and hyperacidosis results. 

The sugar in diabetes is probably first formed from carbohydrates, 
later from proteids, the carbohydrate radicals being probably dis- 
sociated in the proteid disruption. 

Therefore, patients who form sugar after the elimination of sugar 
from the diet furnish a grave prognosis. The chief aim in the treat- 
ment is the almost entire elimination of carbohydrate food or proteid 
food containing glycogen. 1 All cells have a lessened resistance to 
bacteria, as shown by an increased tendency to pneumonia and 
tuberculosis, 2 and a similar predisposition to pyorrhea alveolaris is 
probable. The opsonic index is lowered in all forms of glycosuria 
and, according to Stengel, immunity to bacteria is lowered even in 
experimental cases. 

Symptoms. — Great thirst; frequent micturition (polyuria); in- 
creased amount of urine and the excess of sugar in it; indicated by 
high specific gravity and analysis; excessive appetite; emaciation; 
dyspeptic symptoms; hypochondriasis; insomnia; skin diseases, as 
furunculosis, are common. The glycosuria in diabetes mellitus 
may account for the cervical caries seen in diabetics by introducing 
a factor in lactic acid fermentation, viz., glycogen (starch). (See 
Dental Caries.) 

Peculiar Intrinsic Intoxications. — Without question, intense emotion 
results in the production of intrinsic intoxicants having some influ- 
ence upon metabolism. A most notable example is the classic one of 
a mother, who, shortly after intense rage at an insult, nursed her 
child, with fatal result to it. In another case a child was poisoned by 
the milk of a wet-nurse who spent a night in debauchery (J. Lewis 
Smith). The causes were of slightly different classes, the modus 
operandi much the same. Intense anxiety also has a disturbing 
influence. The nervous influence no doubt alters metabolism, and 
the products act as poisons in a degree corresponding to their 
amount. 

Acid Intoxication. — Many acids may be accumulated in the blood, 
producing the condition known as hyperacidosis or general hyper- 
acidity. The accumulation is probably the result of an increased 
production by metabolism or the incomplete reduction to urea, etc., 
of normal, acid cell excreta. The condition probably arises as the 
result of gastro-intestinal disturbances or altered nerve influence, 
or the failure of function in an organ, as in diabetes in which acidosis 
exists. The acids are carbonic, lactic, sarcolactic, sulphuric, phos- 

1 See works on Practical Medicine. 

2 Stengel, A Text-book of Pathology. 



GENERAL MALNUTRITION 103 

phoric, uric, diacetic, and 0-oxybutyric. The symptoms probably 

result from the acidosis rather than from any one acid. 

Suboxidation always accompanies the condition. Sonic of the 
acids combine with the alkaline elements, and, therefore, reduce 
the normal alkalinity, while the acids left disturb metabolism, thus 
leading to further disturbances. 

Gout. — Gout, or podagra, is a recurrent lion-suppurative arthritis 
associated with the deposits of sodium biurate in the joints, and 
often with constitutional symptoms. It may be acute or chronic, 
by some thought always chronic, with occasional acute manifesta- 
tion. It is largely hereditary or the result of inherited tendency to 
luxurious and indolent life. 

The excessive rise of uric acid from proteid waste is held to be the 
cause of the presence of biurates of sodium, as mechanical irritants 
to the joints, in which, owing to increased age (thirty or over) and 
its tendency to lessened use of joints, a, sluggish circulation with 
increased acidity of the fluids of the part favoring precipitation is 
established. The salts crystallize in the synovial tissue and excite 
inflammation. A slight excess of uric acid in the blood is sufficient 
if the local conditions are as stated. Ebstein claimed that degenera- 
tion or necrotic changes in the tissues cause the precipitation. The 
sluggish circulation leads in this direction. (See Venous Hyperemia 
and Calcareous Infiltration.) 

The conditions leading to a rise of uric acid are many: 

1. Richly cooked foods, especially proteid and sugar, with wines. 

2. Sedentary life combined with the above, or overwork and under- 
feeding, with the use of malt liquors. 

3. Chronic lead poisoning. 

4. Defective elimination; the output in the urine is lessened just 
before the arthritis and increased after it. (Haig.) 

Chronic Gout. — After an acute attack in one joint others may be 
attacked, and tophi (concretions of sodium biurate) form in the ear 
or nasal cartilages, joints, sheaths of tendons, etc. In some cases 
crepitation of the joints may be felt and heard. The joints may be 
distorted and enlargements by the tophi occur; the skin over them 
may be smooth and shiny, but not inflamed. The neighboring veins 
are prominent. 

Constitutional Symptoms. — Complications. — Weakness, anemia, 
cachexia, digestive disturbances, dyspepsia, gastric and intestinal, 
with constipation, failing nutrition, deformity, inability to exercise 
mental irritations and dulness, granular atrophic kidney, cardiac 
hypertrophy and dilatation with arteriosclerosis, chronic gastritis, 
asthma, bronchitis, cerebral or other thrombosis, sciatica, eye-skin 



104 



DISTURBANCES OF NUTRITION 



Fig. 52 



lesions, obesity, diabetes, cholelithiasis, gravel, and vesical calculi. 
(Thompson.) 

Goutiness. — {Gouty Diathesis). — This is the inherited or acquired 
condition underlying the acute and chronic forms of gout, or a 
tendency to gouty symptoms in parts other than the joints, as the 

vital organs, skin, and nervous 
tissues. According to Ewart, " in 
its functional aspect it is due to 
the abnormal acidity of tissue juices, 
while a delicacy of tissues is pro- 
duced or inherited, causing in- 
creased irritability and lowered re- 
sistance." The following diseases 
and symptoms may be associated 
as results, and in themselves show 
the force of Michaels' claim for a 
general hyperacid classification of 
individuals with these symptoms. 
Vascular System. — Arteriosclero- 
sis, an increase of the fibrous 
elements of the arterial walls and 
indicated by their thickening and 
the high tension. 

This induces overwork of the 
heart, resulting in cardiac hyper- 
trophy, and this occurring in the 
coronary arteries produces failing nutrition of the heart and myo- 
carditis with appropriate symptoms. 

Respiratory System. — Asthma, emphysema, and obstinate recurrent 
bronchitis; bronchial catarrh in the young. 

Genito-urinary System. — Uric acid sediment with hyperacidity, 
hematuria, urethritis, oxaluria, albuminuria, glycosuria in some 
cases, menstrual disorders, and uterine and ovarian disturbances. 

Nervous and Muscular Systems.— Neuralgias, muscular soreness, 
lumbago, sciatica, bursitis, sore heels, hemicrania, or migraine, 
neurasthenia. 

Digestive System. — Acid dyspepsia, acid eructation. Tongue may 
show glossitis or leukoplakia, gingivitis, suppurative tonsillitis 
(infection added), bilious headaches, chronic gastritis, colic. 

Skin. — Harsh, dry, tending to eczema, pruritus, urticaria, erythema, 
acne, pityriasis, furunculosis, herpes, exfoliative dermatitis, per-' 
spiration acid. Early gray hair, alopecia. Nails have longitudinal 
stria? and are brittle. 




Tophi of gout. (Ziegler.) 



& 



GENERAL MALNUTRITION 105 

Eyes. Iritis, glaucoma, conjunctivitis. Lesions of retinal vessels, 
retina and optic nerve, keratitis and panophthalmitis. 

These symptoms van- widely in different subjects. 

The chief points of interest to the dentist, apart from diagnosis 
of goutiness, is the peculiar tissue delicacy, and the general hyper- 
acidity as a cause. Without doubt this form of auto-intoxication 
(acidosis) in some cases leads to thickening of small arteries in the 
pericementum, leading to endarteritis obliterans, as shown by Talbot, 
and while not the only form of chronic gingival irritation, is prob- 
ably one cause predisposing to gingival infection leading to the more 
complicated, persistent, and recurrent forms of pyorrhea alveolaris. 

It may be regarded as established that goutiness may exist and 
lead to "declared" gout, or merely act as a chronic tissue irritant. 

Treatment. — The accepted medical therapeutics of goutiness, 
which lies within the special province of the dentist, may well be 
given here. 1 

Diet. — Three moderate meals a day. Eating between meals to be 
avoided. Any meat, except pork, once a day only; fresh fish, eggs, 
lean ham or bacon, oysters or shell-fish at the other meals if desired ; 
oatmeal, hominy, cornmeal, cracked wheat, stale bread and crackers, 
fresh green vegetables and potatoes, leguminous vegetables, apples, 
oranges, cream or other cheese as proteid, soups, tea and coffee in 
moderation, custard and gelatin preparations. Alkaline mineral 
waters, or plenty of plain water, before meals and at bedtime, or 
the tablets of lithium citrate or bitartrate may be taken dissolved 
in w r ater. To be avoided are much meat, sweet dishes and confec- 
tionery, pastry, fried foods, pickles, spices, curry, cakes, griddle 
cakes, alcoholic and malt liquors. 

Hygiene.- — Brisk exercise in the open air to increase oxidation 
and elimination through the induction of perspiration, and Turkish 
baths if no organic disease as of the heart and kidneys exists, and then 
only as advised according to the advance of the disease. Daily cold 
bathing with brisk rubbing ; wearing of woollen clothing. Sea bathing 
or medicated baths. The bowels should be kept freely open with 
cascara sagrada or aloes if necessary. 

Special Therapeutic Indications. — For anemic and neurasthenic 
cases, Fowler's solution, with iron and cod-liver oil, or blood-making 
preparations. 

For feeble digestion: 

1$ — Tincture mix vomicae THx 

Compound tincture gentian or cinchona f5j 

S — Take before meals. 

1 Acknowledgment in part to Thompson's Practical Medicine. 



100 DISTURBANCES OF NUTRITION 

For constipation, cascara sagrada, aloes, Carlsbad water, thialion 
(a laxative salt of lithium). 

For gastric catarrh with constipation and high vascular tension: 

1$ — Sodium sulphate 3J 

S. — Take in a half-tumblerful of hot water one hour before meals, two or three 
times a day. 

For persistent high vascular tension: 

Nitroglycerin gr. T ^„ every three hours. 

Or, 

Sodium nitrate gr. iij three times a day. 

Or, 

Chloral hydrate gr. v three or four times a day. 

Lithemia. — This is a condition occurring in individuals who 
overfeed, drink too little fluid, exercise little, and are under various 
nervous strains or overwork. A neurotic disposition and stimulants 
enhance the disturbances of nutrition. 

Cold weather, adding to the above a lessened perspiration and 
increase of work by the kidneys, increases the difficulty. Tobacco 
and alcohol increase the ill effects. 

There may be no symptoms of gout in even marked cases. There 
is acidosis with lithuria (uric acid in the urine) or oxaluria; eventually 
renal, vascular, and hepatic scleroses develop, together with liability 
to localized inflammation chiefly in serous membranes, as the pleura 
or synovia. 

The hypothesis is that uric acid or some proteid toxin irritates 
the capillaries to contraction, thereby raising vascular tension, and 
by this twofold toxic and mechanical action causing arteriosclerosis, 
which in turn induces cardiac hypertrophy, sclerotic kidney changes, 
and vascular hepatic cirrhosis. It tends toward neurasthenia. 

Symptoms. — Nervous Symptoms. — Vertigo, tinnitus aurium, in- 
somnia, restlessness, burning or pricking sensation in the palms or 
soles, darting pains in the limbs, hebetude of mind, hypochondriasis, 
hemicrania, or diffuse basilar or frontal headache, general nervous 
irritability. 

Digestive Symptoms. — Lost or capricious appetite; coated red or 
dry tongue, often fissured; aphthous ulcers, thirst, metallic taste in 
the mouth, pyrosis, hiccough, gastric oppression, nausea, gastralgia, 
vomiting, flatulence; constipation or irregular, dark-colored, frothy 
stool; palpitation of the heart (an hour or two after meals), hepatic 
tenderness. 



GENERAL MALNUTRITION 107 

Urine. Scanty, dark, strongly acid, of high specific gravity, with 
often brick-dust sediment of urates. Perhaps temporary albuminuria ; 
perhaps inflammation of urinary passage. 

Skin. — Eczema, pruritus, urticaria or lichen. 

Therapeutics. The condition of life should be reversed as to previous 
eating and drinking, and exercise to avoid the overstimulation by 
proteid food waste and to increase elimination. Stimulants are to 
be avoided, sodium phosphate given for its action upon the liver in 
promoting the excretion of bile, and also for its mildly cathartic 
effect. It also furnishes an element for regeneration of nervous 
tissue, and renders the body fluids more alkaline. Lithium prepara- 
tions are of little value. Potassium acetate, bicarbonate, and citrate 
are useful. The bowels are to be kept open. Headaches may be 
relieved by: 

fy — Phenacetin gr. xxxvj 

Salol, 

Caffein aa gr. xxiv 

M. and ft. capsulse no. xii. 

S. — A capsule three or four times a day. 

For the neurasthenic cases treat w T ith arsenic and glycerophos- 
phates. 

The diet is to be regulated as in goutiness. The use of much fat, 
meats, or carbohydrates is to be avoided, to lessen the necessity 
for oxidation and for w^ork by the liver. The use of a largely vege- 
table diet,. to render the body fluid more alkaline. Plenty of water 
between meals, to flood the system. Hygiene, rest, and exercise, as 
in goutiness. 

Rheumatism. — Rheumatism is an acute fever, probably of infective 
origin, characterized by constitutional toxic symptoms, inflammation 
of the joints, muscles, serous membranes, skin, or even tonsils. It 
may be classified as acute, chronic, or muscular rheumatism. 

Etiology of Acute Rheumatism. — It may be transmitted to the 
new r born, or a constitutional tendency to it may be inherited. It is 
most common to young adults (fifteen to twenty-five years), but no 
age is exempt. It is most common in males. 

Climate, exposure to cold, injuries and overwork of parts, occupa- 
tion inviting exposure to hardships, chronic alcoholism, nervous shock, 
debility, starvation, anemia, and chorea are other predisposing causes. 

The exciting cause is supposed to be largely due to the Diplo- 
coccus rheumaticus, having its origin in some focus of infection, as 
the tonsil or gum margin. The streptococcus or pneumococcus may 
be absorbed from some focus of infection and produce metastatic 
joint inflammation similar to rheumatism and be isolated from the 



108 



DISTURBANCES OF NUTRITION 



blood or joints of rheumatic patients, but it is also induced by a diet 
of meat or the fermentation produced by overuse of sugar and 
starches, causing a rise of lactic or uric acid in the blood. 

Clinical History. — It presents the following clinical difference from 
acute gout: 1 





Acute gout. 


Acute rheumatism. 


Exciting cause 




Often errors in eating and drinking. ! 


Sometimes cold and damp. 


First attack . 




Commonly in one great toe. 


Commonly in large joints. 


Later attacks 


; \ 


Both toes, fingers, knees, etc. 


Rare in toes, often shoulder 
or hip. 


Appearance of 


joint 


Color dark red, shiny, and tense. 


Lighter red. 


Pain . 




Worse at night or early morning, 


Migratory from joint to 






localized. 


joint. 


Subsidence . 




Leaves thickening and deformity 
with repeated attacks. 


Leaves normal joints. 


Tophi . . 




In lobes of ear, finger-joints, etc. 


Never present. 


Age and sex . 




Common in middle-aged men; very 


Common in young persons, 






rare in children. 


children, and women. 


Effect of treatment . 


Salicylates have but little effect; 


Salicylates have marked 






colchicum marked effect. 


effect; colchicum no 








effect. 



Symptoms. — Pain and inflammation of joint, which may be pre- 
ceded by headache, indigestion, constipation, lassitude, muscular 
aching, chilliness, mild inflammation of tonsils, pharynx, and larynx. 
Tongue coated, pale, and indented by the teeth; breath foul. Fever 
103° or 104° F., sometimes hyperpyrexia. Sweating during the 
height of convalescence, with acid odor from decomposition of fatty 
acid, but may be neutral or alkaline in parts of same person, therefore 
not an effort at elimination of acid. 

Saliva. — Acid, excess of potassium sulphocyanid. 

Urine. — Hyperacid, urates increased, chlorids diminished, uric 
acid abundant, sometimes albuminuria. 

Heart. — Pericarditis and endocarditis in one-fourth of all cases. 

Mind. — Clear except in hyperpyrexia. 

Skin. — Urticaria, petechia?, ecchymoses, purpura, eczema at times; 
subcutaneous nodules in youth. 

Complications.— Conjunctivitis occasionally; chorea frequently. 

Prognosis. — Uncertain as to period before recovery; relapses, or 
recurrence common. 

Therapeutics. — Sodium salicylate and oil of gaultheria, internally, 
relieve the pains and inflammation. Cold baths to reduce the tem- 
perature. Blisters as counterirritants; protection from jarring by 



Thompson's Practical Medicine. 



GENERAL MALNUTRITION L09 

cotton and fenders; guaiacol with glycerin, oil of wintergreen, etc., 
as local lotions. The diet is much the same as in gout. 

Chronic Rheumatism.— This form has much the same etiology, 
but is more common after the fortieth year. It appears in much- 
used joints, and is most common in females. 

Morbid Anatomy. — Fibrous thickening and contraction produce 
moderate thickening and distortion of joints; atrophy of muscles 
about joints may occur. 

Symptoms. — Symptoms are of slow onset; general health good 
unless inability to exercise produces alteration. Pain absent except 
when joint is overworked or in damp weather. The fingers may be 
deflected laterally and flexed by contraction of tendons. Febrile 
attacks, 101° F., occur from time to time, but the urine is normal. 

Prognosis. — Disease progressive; no recovery, but temporary im- 
provement by treatment so that the joints may remain quiescent 
for years. Never fatal. 

Systemic Therapeutics. — Simple alkalies or alkaline waters, arsenous 
acid, 20 gr. t. i. d., cod-liver oil for debilitated and anemic, Carls- 
bad salts or sodium phosphate for constipation. 

Local.— Drenching with hot (105° to 110° F.) and cold (70° F.) 
water alternately, followed by massage and wrapping the joint in 
flannel. Sweating in an inclosing box with hot air, 240° or 250° F., 
followed by Swedish movements. The lotions used for acute rheu- 
matism are also used. The diet is much the same as for goutiness. 

Muscular Rheumatism. — In this form of rheumatism the dis- 
turbance is in the muscles, with little constitutional disturbance. 
The essential lesion is probably an inflammation of the muscles, 
though the nerves may suffer. 

Symptoms. — Local tenderness and pain increased by every con- 
traction of the muscle. Pain stationary, worse by night and during 
barometric disturbances; oxaluria in some cases. 

Scorbutus (Scurvy). — This is a subacute or chronic disease, char- 
acterized by inanition, anemia, and asthenia, with purpura and a 
tendency to swelling of the gums. 

While of doubtful origin, defective hygiene and the use of improper 
foods, especially the lack of fresh vegetables and fruits, and the use 
of salted foods, the improper absorption of food owing to chronic 
intestinal maladies, as dysentery, or to cachexias, as in malaria, 
cancer, and syphilis, are the chief causes, though infection has been 
held to act upon those debilitated by the above causes. In young 
children it is due to the use of proprietary foods instead of fresh 
food, and appears mostly from the eighth to the twelfth month, 
rarelv before the sixth or after the sixteenth month. 



110 DISTURBANCES OF NUTRITION 

The circulation is feeble and the blood impoverished. 

The gums are red and swollen, protrude over and between the 
teeth if present, and bleed; the breath is offensive, owing to putre- 
faction of the blood. 

The stomach shows great irritability, and there is thirst and craving 
for acid foods. 

The joints are swollen and painful, owing to the hemorrhages. 

The urine is high colored; the acidity and temperature lowered. 

Treatment. — As a prophylactic and cure, lime, lemon, or orange 
juice, together with the use of fresh vagetables and fruit in adults, 
or their juices in infants. Fresh milk modified, white of egg, and 
beef juice, or breast feeding, are to be substituted for proprietary 
foods or table feeding in infants. 

Rachitis (Rickets). — This is a disease found in infants, develop- 
ing typical deformities in the bones, and due to a deficiency of 
lime salts in them, in turn probably due to an absorption of that 
present, by hyperemic tissue present, and a diminution in the deposi- 
tion of a fresh supply. There is usually, also, hypertrophy of the 
liver and spleen. The prolonged lactation of the child upon unfit 
milk, poor in fat, and the overuse of proprietary foods lacking the 
proper food elements, as farinaceous food or exclusively a condensed 
milk diet. The teeth develop slowly and are apt to be of faulty 
structure. The general line of treatment is much the same as for 
scorbutus. 

Neurasthenia. — This is a condition of nervous exhaustion, no 
reserve nerve matter being held for even slight effort. It is often 
accompanied by nervous excitability, insomnia or disturbed sleep, 
apprehension, melancholia, failure of appetite, and feeble digestion. 

Nervous energy is lost and irritability remains. It may be caused 
by continued excitement or overwork of the nervous system, and 
responds to rest, regulated diet, general tonics, treatment by glycero- 
phosphates of lime and soda in the serious cases, while in mild cases 
exercise in the open air, baths, sea or mountain air, combined with 
the tonic treatment and abstinence from stimulants, effect a cure. 1 
In view of demonstrations upon animals that nerve tissue is actually 
used up in nervous energy, the above treatment probably permits 
a gradual restoration of the elements of nerve tissue. 

Oxaluria. — The increase of sodium and calcium oxalate crystals 
in the urine indicates : 

1. That food rich in oxalic acid (as tomatoes or rhubarb) has 
been used in increased quantity. 

1 See Thompson's Practical Medicine. 



GENERAL MALNUTRITION 111 

2. That intestinal fermentation is existent and forming it from 
glucose. (Baldwin.) 

3. That intrinsic increased production of oxalic acid by oxidation 
of uric acid, in turn derived from the purin bases of the nucleins, 
and niicleo-albnmin of the tissues is present. 

It frequently accompanies the increase of uric acid in the urine, 
and is regarded by Simon 1 as due to impairment of normal oxidation 
processes in the liver. Thus it may be found in goutiness and lithe- 
mia. It is also associated with dyspeptic and nervous symptoms, 
producing a condition known as oxalic acid diathesis. It also 
sometimes accompanies diabetes. 

Continued oxaluria may result in the formation of calcium oxalate 
calculi. It is frequently associated with nervous irritability, hypo- 
chondriasis, and neurasthenia. Oxalates are found in the urine and 
saliva. (See p. 96.) 

Phosphaturia. — The tribasic, phosphoric acid, H 3 P0 4 , is a normal 
product of metabolism, and like other acids combines with salts 
before elimination. Its alkaline combinations are sodium phosphate, 
Xa 3 P0 4 ; calcium phosphate, Ca 2 (P0 4 )2; and magnesium phosphate, 
Mg 3 (P0 4 ) 2 , which may also be found in alkaline urine. Its neutral 
combinations are di-sodium hydrogen phosphate, Na 2 HP0 4 ; calcium 
hydrogen phosphate, CaHP0 4 ; and magnesium hydrogen phosphate, 
MgHP0 4 , all found in the blood and in neutral urine. Its acid 
combinations are sodium di-hydrogen phosphates, NaH 2 P0 4 , and 
calcium di-hydrogen phosphate, Ca(H 2 P0 4 ) 2 , found in acid urine, 
and to which the normal acidity is partly and chiefly due. 

Ammonium magnesium phosphate (NH 4 MgP0 4 +6H 2 0) or triple 
phosphate is also found. 2 

Many of the phosphates are derived from the food, but some are 
formed by proteid catabolism; one-third of all excreted is eliminated 
in the intestinal secretion; some are eliminated in the saliva, as shown 
by the formation of salivary calculi. In diseases requiring increased 
phagocytosis, as febrile conditions, the elimination of phosphates 
falls, the phosphates probably being utilized in the formation of 
leukocytes. The excretion is increased in diabetes and tuberculosis. 

A very large increase in the total amount of phosphates eliminated 
(7 to 9 grams in twenty-four hours) is called phosphatic diabetes, 
and has been associated with four classes of symptoms: 

(a) Cases with marked polyuria and marked nervous symptoms. 

(6) Cases preceding or accompanying pulmonary diseases, espe- 
cially tuberculosis. 

1 Simon, Clinical Diagnosis. 2 Kiike's Physiology. 



112 DISTURBANCES OF NUTRITION 

(c) Cases in which phosphaturia alternates with or coexists with 
glycosuria. 

(d) Cases in which oxaluria, polyuria, and slight albuminuria are 
present, and in which some relationship with gout exists. 

An increase in the amount of phosphates in the blood tends to the 
production of calculi. 

As nerve tissue contains a considerable amount of lecithin or phos- 
phorized fat essential to it, excessive drain upon this may result 
in a loss of this substance by catabolism, with loss of phosphates 
doubtless masked by the preponderance of phosphates derived from 
the food. 

This is borne out by the beneficial use of glycerophosphates of 
lime and soda, rest, and general tonic treatment in neurasthenia. 
(See p. 110.) 

Albuminuria. — The presence of albumin in the urine may be 
either (1) transitory, remittent, or cyclic (recurring with regularity), 
as the result of functional disturbances, as anemia, adolescence, in 
general malnutrition, after severe exercise or cold baths; or (2) due 
to organic disease of the kidney, as acute and chronic nephritis, 
renal arteriosclerosis, and amyloid degeneration of the kidhey; or 
(3) to fevers, as typhoid and yellow fever, and is due to the presence 
of bacterial toxin in the blood; or (4) to circulatory disturbances, as 
organic heart disease, or to local circulatory disturbances, as com- 
pression of renal veins by a pregnant uterus; or (5) to impeded out- 
flow of urine; or (6) to hemic changes, increasing the diffusion of 
albumin, as in scurvy, leukemia, pernicious anemia, jaundice, and 
diabetes ; or (7) to toxins in the blood other than febrile, as turpentine, 
salicylic acid, phosphorus, arsenic, etc., probably producing circu- 
latory disturbances and irritation of glandular epithelium of the 
kidneys; or (8) to neurotic disturbances, as epilepsy; or (9) to in- 
gestion of excessive amounts of cheese, eggs, and other albuminous 
food; or (10) to accidental admixture after urine excretion by the 
kidneys 1 

It is, therefore, like oxaluria and phosphaturia, more a symptom 
than a disease. 

1 Simon, Clinical Diagnosis. 






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OftAWN BY J.N.Z. CHASC 



BLOOD. 

(Ehrlich triple stain.) 
(Prepared by Dr. I. P. Lyon.) 

Fiy. I. TYPES OF LEUCOCYTES. 

a. Polymorphonuclear Neutrophile. b. Polymorphonuclear Eosinophile. c. Myelocyte 
(Neutrophilic), d. Eosinophilic Myelocyte, e. Large Lymphocyte (large Mononuclear). 
/. Small Lymphocyte (small Mononuclear). 

Fig. II. NORMAL BLOOD. 
Field contains one neutrophile. Reds are normal. 

Fig. III. ANEMIA, POST-OPERATIVE (secondary). 

The reds are fewer than normal, and are deficient in haemoglobin and somewhat 
irregular in form. One normoblast is seen in the field, and two neutrophils and one 
small lymphocyte, showing a marked post-haemorrhagic anaemia, with leucocytosis. 

Fig. IV. LEUCOCYTOSIS, INFLAMMATORY. 

The reds are normal. A marked leucocytosis is shown, with five neutrophiles and 
one small lymphocyte. This illustration may also serve the purpose of showing the 
leueoeytosis of malignant tumor 

Fig. V. TRICHINOSIS. 
A marked leueoeytosis is shown, consisting of an eosinophilia. 

Fig. VI. LYMPHATIC LEUKEMIA. 

Slight anaemia. A large relative and absolute increase of the lymphocytes (chiefly 
the small lymphocytes) is shown. 

Fig. VII. SPLENO-MYELOGENOUS LEUKAEMIA. 

The reds show a secondary anaemia. Two normoblasts are shown. The leueoeytosis 
is massive. Twenty leucocytes are shown, consisting of nine neutrophiles, seven myelo- 
cytes, two small lymphocytes, one eosinophile (polymorphonuclear) and one eosinophilic 
myelocyte. Note the polymorphous condition of the leucocytes, i.e., their variations 
from the typical in size and form. 

Fig. VIII. VARIETIES OF RED CORPUSCLES. 

a. Normal Red Corpuscle (normocyte), b, c. Anaemic Red Corpuscles, d-g. Poikilocytes. 
h. Microcyte. i. Megaloeyte. j-n. Nucleated Red Corpuscles. j,k. Normoblasts. I. Micro- 
blast. m,n. Megaloblasts. 



CHAPTER V. 



DISTURBANCES OF THE VASCULAR SYSTEM. 



A suitable amount and quality of blood normally flows through 
the circulatory apparatus, and is in close relation to processes of 
nutrition. 

The amount of blood in the vessels may be increased (plethora), 
though not permanently. It may be decreased rapidly in quantity, 
as by hemorrhage, or its red corpuscles may be gradually lessened 
in number (acute or chronic anemia). The proportion of white cor- 
puscles to red ones may be increased abnormally (leukemia). The 
hemoglobin of red corpuscles may be deficient (chlorosis). Locally 
the amount of blood in a part may be increased (hyperemia or 
inflammation) or diminished (ischemia). 

Normally the blood contains floating in the plasma 5,000,000 red 
corpuscles, or erythrocytes, and from 5000 to 10,000 (1 to 500 red) 
white corpuscles, or leukocytes, to each cubic millimeter. (See Plate, 
Fig. II.) A marked increase in the number of erythrocytes is termed 
polycythemia; a marked decrease, oligocythemia. The temporary 
increase in number of white corpuscles is leukocytosis; a persistent 
increase, leukocythemia or leukemia. 

The blood corpuscles may be classified as follows: 



See Plate, 
Fig. 53 Fig. VIII 



Erythrocytes (non-nu- 
cleated red corpuscles) 



1, 2, 3, 4. 



Normal to 
blood. 

I Microcytes (small size) h 

Pathological 1 Macrocytes (large size) 
indicators. | Megalocytes (very large size) ...... i 

{ Poikilocytes (irregular form) d e f g 

Erythroblasts (nucleated ( r 

red corpuscles derived J Pathological ! 
from red marrow of ] indicators. ] 



bones) 



°'i 



Normocytes (normal size) 



Normoblasts (normal size) 
Microblasts (small size) 
Megaloblasts (large size) , 



I 



Leukocytes (white cor- 
puscles) . . . . 



Normal to 
blood. 



Pathological 
indicators. 



See Plate, 
Fig. 53 Fig. I 

I Lymphocytes (small) 22% 5 / 

Lymphocytes (large) 6 " 6 e 

Polymorphonuclear neutrophils . . 70 " 7 a 

Polymorphonuclear eosinophiles 2 " S b 



Basophilic leukocytes or mast cells. 
Neutrophilic myelocytes from bone-marrow . 
Eosinophilic myelocytes 

(113) 



114 



DISTURBANCES OF THE VASCULAR SYSTEM 
Fig. 53 




stf • • •ft? 





Normal blood (triacid stain): 1, normal red cell, flatly spread and evenly stained; 
2, normal rouleau; 3, normal red cells varying slightly in size, thickly spread, show- 
ing central clear areas; 4, normal red cell, of slightly altered shape; 5, lymphocyte, 
medium size; 6, large mononuclear leukocyte, incurved nucleus; 7, polynuclear 
neutrophile leukocyte; 8, eosinophile leukocyte. Separate nuclear lobes. (Schmaus 
and Ewing.) 

ANEMIA. 

Anemia is a condition in which the blood is lessened in quantity 
or partly deprived of its essential constituents — i. e., red corpuscles 
and hemoglobin — in consequence of which the tissues receive less 
oxygen and the general nutrition is impaired. 

Acute Traumatic Anemia occurs as a result of copious hemor- 
rhage. The individual becomes temporarily pale and weak. The 
arterial pressure is lessened, the circulation slowed, and the pulse 
is frequent and small. Recovery is, as a rule, prompt, the water 
being first restored and later the corpuscles being regenerated. 1 
Frequent hemorrhages cause the blood to become watery and debility 
results from impaired nutrition. (See Plate, Fig. III.) 



Ziegler, General Pathology 



ANEMIA 115 

Symptomatic Anemia. — A diminution in the number of red cor- 
puscles may occur as a result of protracted overwork, anxiety, study, 
or long-continued illness, such as a fever. 

The number of red blood corpuscles may be reduced to one-half the 
normal amount, and there is a corresponding debility. The condition 
may disappear with appropriate removal of the cause. 

Chlorosis. — This is a form of anemia occurring, for the most part, 
in girls and young women, and characterized by a great deficiency 
in the hemoglobin of the red corpuscles without a corresponding 
reduction in the number of the red corpuscles. In the watery blood 
very small red corpuscles (microcytes) are seenf also a few very 
large ones (macrocytes), and some of irregular outline (poikilocytes). 1 
Myelocytes are occasionally seen. (Stengel.) The pathology is 
uncertain. If prolonged, the red corpuscles may sink in numbers 
to 3,000,000 or 2,000,000 per cubic millimeter and 20 per cent, of 
hemoglobin. 

Being, as a rule, readily cured by a course of iron, it is inferred 
that the body is starved of iron, an essential constituent of hemo- 
globin. It is often associated with gastric disturbances, constipation, 
defective hygiene, and irregular habits, which apparently have a 
causal relation. The skin and mucous membranes are pale and have 
a slightly greenish tinge. 2 In recovery the number of corpuscles is 
first increased, then the hemoglobin. 

Leukocytosis. — This is not a form of anemia, but a temporary 
increase in the number of multinucleated leukocytes, apparently, 
derived from the lymphoid structures of the body in response to 
some demand for leukocytes. Thus it occurs after a full meal, in the 
later months of pregnancy, in acute fevers, in tuberculosis, and in 
conditions accompanied by suppuration. 3 Its presence during the 
course of surgical disease has been held to be diagnostic of pus forma- 
tion 4 — e. g., in abdominal surgery from 8000 to 20,000 per cubic 
millimeter. (See Plate, Fig. IV.) 

Leukemia. — Leukemia is a disease characterized by a consider- 
able increase in the number of white corpuscles of the blood, by a 
diminution in the number of the red corpuscles, and by enlargement 
of some of the lymphatic organs. The proportion of one white to ten 
red corpuscles is common (1 to 5 often, occasionally 1 to 1). The 
spleen may be hypertrophied (splenic leukemia). The lymphatic 
glands may be hypertrophied (lymphatic leukemia). In these latter 
cases the blood contains an excess of uninuclear leukocytes. It is rare 

1 Green, Pathology and Morbid Anatomy. 

2 Ibid. 3 Ibid. 
1 Cabot. Boston Medical and Surgical Journal. 



11G DISTURBANCES OF THE VASCULAR SYSTEM 

except when combined with other forms. When the marrow of bones 
is hypertrophied (myelogenic leukemia) large mononuclear leukocytes 
with neutrophile granules are found 1 (myelocytes) and the lympho- 
cytes and polymorphonuclear forms are increased. 2 The blood con- 
tains toxic substances generated by the destruction of leukocytes, 
xanthin bodies, and acids (lactic, acetic). The urine frequently 
contains an excess of xanthin bases and lactic acid. (See Plate, 
Figs. VI and VII.) 

Pernicious Anemia. — This is a comparatively rare but generally 
fatal disease, characterized chiefly by a great fall in the number of 
red corpuscles to one million or less per cubic millimeter, those 
remaining being altered in form and size and showing evidences of 
degeneration. The total hemoglobin is reduced, but the relative 
amount may be increased. Degeneration is shown by peculiarities 
of staining. Normal red corpuscles (normocytes), nucleated red 
corpuscles (megaloblasts), large nucleated red corpuscles (giganto- 
blasts), microcystes, and poikilocytes are found. The blood platelets 
and leukocytes are somewhat diminished. 3 The oxygen-carrying 
power is markedly lessened and all tissues suffer from malnutrition. 
The power of coagulation of the blood is lessened. Marked fatty 
degeneration of the heart muscles is apt to occur 4 as well as fatty 
changes in the kidneys and liver. 

The causes are obscure, but gastro-intestinal disorders, intestinal 
parasites, pregnancy and lactation, hemorrhages, malaria, syphilis, 
tuberculosis, and infections are the chief causes supposed to produce it. 

Aplastic anemia is a severe type of progressive pernicious anemia, 
in which the bone-marrow fails to develop myelocytes and erythro- 
blasts owing to lack of marrow cells (hypoplasia of bone-marrow.) 

COAGULATION OF THE BLOOD. 

The blood when drawn from the body or in contact with a wounded 
surface of injured vessel wall undergoes a process of solidification 
called coagulation. The nature of the process is in some doubt, but 
it is now thought that the injury of white corpuscles, blood platelets 
and tissue cells liberates a ferment called thrombokinase, which with 
the aid of calcium salts converts the prothrombin in the blood plasma 
(thrombogen) into thrombin. This combines chemically with the 
fibrinogen of the plasma to form fibrin which takes the form of a 

1 Ziegler, General Pathology. 

2 Stengel, A Text-book of Pathology. 

3 Green, Pathology and Morbid Anatomy. 

4 Ibid. 



rOAGULATIOX OF THE BLOOD 



117 



network, in the open spaces of which the corpuscles are entangled 
(Fig. 54). 1 Coagulation may occur in the living vessel, as a throm- 
bus, or in the interstitial tissue, 
lui - 54 as in inflammation and infarc- 

\ \ w tion * 

^^bg2$^ Thrombosis. — The formation 

-C x - of thrombi or clots within the 



Fig. 55 




Fibrin filaments and blood tablets. 
A, network of fibrin, shown after 
washing away the corpuscles from a 
preparation of blood that has been 
allowed to clot; many of the fila- 
ments radiate from small clumps of 
blood tablets; B (from Osier), blood 
corpuscles and elementary particles 
or blood tablets within a small vein. 

Fig. 56 




A thrombus in the saphenous vein, 
showing the projection of the conical 
end of the thrombus into the femor.il 
vessel: S, saphenous vein; T, throm- 
bus; C, conical end projecting into 
femoral vein. At v, v, opposite the 
valves, the thrombus is softened. 
(Virchow.) 




Diagram to show phenomena of 
venous thrombosis: v, v, valves of veins; 
a, b, primary thrombus (white) ; c, d, 
e, f, 0, secondary white thrombi con- 
nected with primary white thrombus 
by various red thrombi; h, piece of white 
thrombus becoming detached by blood 
current. (Green, modified from Thoma.) 



living vessel may occur in the heart, arteries, veins, or capillaries. If 
the blood stream be somewhat retarded, an increased number of 
white corpuscles and blood platelets occupy the peripheral zone and 

1 Howell, Text-book of Physiology. 



US 



DISTURBANCES OF THE VASCULAR SYSTEM 



adhere to the vessel wall. If the vessel wall be injured, the blood 
platelets become attached to it. With these platelets the white 
corpuscles and sometimes the red become deposited. Fibrin forms 
and the corpuscles are included. The thrombus is red when red 
corpuscles are included in it; white when only white corpuscles are 
present. The causes of thrombosis are these: (1) a retardation of 
the blood current at some point from some cause; (2) local changes 
in the walls of the vessels and (3) probably pathological changes in 
the blood. 1 

Fig. 57 




Embolus impacted at the bifurcation 
of a branch of the pulmonary artery, 
showing the formation of thrombi be- 
hind and in front of it, and the exten- 
sion of these as far as the entrance of the 
next collateral vessels: E, embolus; t, 
t', secondary thrombi. (Virchow.) 




Diagram of a hemorrhagic infarct: 
a, artery obliterated by an embolus (e) ; 
v, vein filled with a secondary throm- 
bus (th); 1, centre of infarct which is 
becoming disintegrated; 2, area of 
extravasation; 3, area of collateral hy- 
peremia. (O. "Weber.) 



Older thrombi are firmer than those recently formed. Thrombi 
are also formed in the capillaries, a circumstance which favors the 
spontaneous cessation of hemorrhage. They may form in the vessels 
in inflammation. Remaining in the situations in w T hich they were 
formed, they either undergo simple or puriform softening or are 
calcified, or are resorbed and replaced by connective tissue. (See 
Regeneration.) The calcified varieties are called phleboliths in the 
veins; arterioliths in the arteries. In senile gangrene a thrombus 
may extend a great distance. 

Embolism. — Portions of the softened varieties of thrombi may 
become detached and float about in the blood; these are called 
emboli. Other foreign substances may act as emboli — e. g., air or 
fat globules. In important parts it may cause local anemia, necrosis, 
or slow 7 or rapid death. 



Ziegler, General Pathology. 



COAGVLAflON OF THE HLOOl) 11!) 

If the thrombus be septic, as in the case of puriform softening, the 

emboli may lodge in small vessels and cause secondary septic disease 
processes, as, for example, in the cases of pyemia accompanied by 
infarctions. 

Infarction. — When an embolus occludes a terminal artery, that 
is, an artery whose branches spread like those of a tree without 
anastomosis, the part first becomes ischemic, but soon the backward 
pressure from the vein upon the blood in the capillaries causes an 
extravasation of blood into the interstitial tissue of the wedge-shaped 
area, forming what is called a hemorrhagic infarct. A clot forms, 
degeneration of the clot occurs, and if aseptic it is absorbed and 
replaced by connective tissue (see Regeneration); if caused by a 
septic embolus, it may r be involved in the resulting septic process — 
e. g., in pyemic metastatic abscess. Infarcation has been held by 
Black to occur in the dental pulp. A demonstration has been made 
by Hopewell-Smith. (See Diseases of the Pulp.) (See Fig. 58.) 

Hemorrhage. — By hemorrhage is meant the escape of blood from 
the vessels. It may be arterial, venous, or capillary. If the vessel 
is ruptured, it is hemorrhage by rhexis. If it occurs by diapedesis, 
as in infarction (from veins and capillaries only), it is hemorrhage 
by diapedesis. The diapedesis occurs through the capillary wall 
rather than the stomata ; pressure is the cause. Hemorrhage usually 
ceases spontaneously through thrombosis. 

If hemorrhage occurs into, the tissues it receives the following 
designations, the escape itself being called an effusion or extrava- 
sation : 

Ecchymosis, an effusion of moderate extent into tissue beneath a 
surface, as into subcutaneous tissue. 

Petechia the same, but small and circumscribed ; when an extensive 
area is involved it is termed a suffusion. 

Infarction, when the area involved is that supplied by terminal 
and non-anastomosing arteries. 

Hemorrhage involves an injury to vessels by traumatism, or 
disease rendering them incapable of retaining the blood, or by 
increased pressure, as in violent exertion, or in congestion of local 
vessels, as in venous hyperemia, or as the result of diminished 
atmospheric pressure, as in high altitudes. The extra vasated blood 
corpuscles may be disintegrated into pigments (see p. 88), and be 
absorbed or deposited in the tissues, as in a bruise; or excite inflam- 
mation or cyst formation (extravasation cyst). Acute hemorrhages 
or repeated extravasations lead to anemia (which see). 

Hemorrhagic Diathesis. — This is a condition, largely hereditary, 
in which coagulation does not close wounds readily, and ordinarily 



120 DISTURBANCES OF THE VASCULAR SYSTEM 

trivial wounds may, in spite of surgical aid, induce death by hemor- 
rhage. Hereditary hemorrhagic diatheses (hemophilia) is usually 
transmitted through the female to the male descendants — i. e., from 
grandfather to grandson through the grandfather's daughter — and 
seven or more generations of hemophiliacs have been recorded. 1 
Males suffer more than females in the ratio of about 11 to 1. 

In a family of 207 members, in four generations, 37 were hemo- 
philics, all of the male sex; almost half died from hemorrhages, 
usually in infancy, while the tendency to bleed lessened as they 
grew older. 2 

According to Legg, 3 "It is of three degrees of severity: 

"1. Characterized by external and internal bleedings of every 
kind, and by joint affections. 

"2. By spontaneous hemorrhages from mucous membranes, but 
no traumatic bleeding or ecchymoses, and no joint affections. 

"3. A tendency simply to ecchymoses. The first seen most 
frequently in men, the second in women; the third may appear 
in either sex." 

The joint affections are due to hemorrhage, and simulate rheumatic 
affections. Hemophiliacs are apt to be thin-skinned, neurasthenic, 
and liable to sudden flushings and vasomotor disturbances. 4 Blondes 
suffer more than brunettes. 5 

The injured part may bleed from the first, or a normal clot may 
form and secondary hemorrhage or capillary oozing occur. Death 
may rapidly occur, or the patient bleed to fainting or until almost 
dead, and hemorrhage then cease. This may require any period, 
even weeks. One case is said to have continued for a year. 6 

The pathology of the condition is uncertain. Fillebrown 7 reports 
a fatal case in which the arteries were excessively thin. Porter points 
out that the blood may clot in the receptacle, yet not in the small 
vessels of the wound, and infers that some hereditary deficiency exists 
which interferes with the action of the vasoconstrictors. 

Hemophilics usually manifest a history of bleeding before puberty, 
and hemophilic infants have died from hemorrhage due to gum- 
lancing, circumcision, etc. Certain surgical cases in which secondary 
hemorrhages have been due to the action of the continuous use of 
acetanilid have been reported. The therapeutic measures indicated 
are hemostatics internally, local styptics, compresses, etc. Potassium 
permanganate, made into a paste with vaselin, is recommended as a 

1 Porter, International Dental Journal, 1900. 

2 Losser, International Journal of Surgery. 

3 Musser, Medical Diagnosis. 4 Porter, Loc. cit. 

5 Thompson, Practical Medicine. 6 Scott, Dental Cosmos, 1912, p. 60. 

7 International Dental Journal, 1900. 



COAGULATION OF THE BLOOD 121 

styptic. A solution of calcium chlorid, gr. xxx, and water, 5j, has 
been used on cotton with satisfaction. 

In case of tooth extraction reimplantation has been urged, but 
must be done under aseptic precaution, as any infected dead pulp or 
even a root infected by contact with the hands, saliva, etc., may 
substitute a condition almost as bad as the hemorrhage. 

In a severe hemorrhage upon the palate, as after lancing an 
abscess, finger pressure may be used, or, if necessary, a vulcanite 
plate may be made to produce the necessary pressure. 1 

Sodium sulphate, gr. iss, even' two hours, has been of service in 
marked hemorrhages. 2 

The following is useful: 

R- — Calcii chloridi gr. lxxv to cl 

Syrupi ruenthse 3v 

Aquae destillatae fgiiiss — M. 

Tablespoonful doses or a clyster containing 75 grains calcium chlorid and a few- 
drops of tincture of opium. 3 

For persistent postextraction hemorrhage, Endelmann has recom- 
mended : 

R— Vini ergotse, U. S fSij 

Sig. — Teaspoonful every two hours. 

Dilute sulphuric acid and Hydrastis canadensis are used, also 
gelatin locally and by injection. 4 The gelatin may contain tetanus 
spores and should be sterilized for forty minutes or longer at 100° or 
120° C. a Suprarenal extract, gr. xx to 5 j, topically, gr. x by mouth, 
every four hours, is also useful. Absolute quiet and the withholding 
of food for two days; the hunger to be relieved by small doses of 
opium and thirst by iced water in small quantities. 6 The acute 
anemia induced requires treatment. 

Individuals known to be hemophilic should live a hygienic life and 
avoid all injuries, however slight, possible to avoid, in the hope of an 
eventual outgrowing of the condition. If operation be unavoidable, 
they should be treated w T ith calcium chlorid, gr. iij ter in die, for not 
more than four days, as thereafter the coagulability of the blood is 
decreased. 7 Much larger doses, gr. xxx to § j, have been satisfactorily 
given for cure and prevention. 8 Scott states three cases in w T hich 
it was of no value, and suggests strontium lactate 15 -grain dose to 
be used by the patient. Calcium lactate, first dose 20 grains, five 

1 Joly, see Dental Cosmos, 1909, p. 488. 

2 Reverdin, Dental Cosmos, February, 1904, p. 162. 

3 Rosod, New York Medical Journal. 4 Hare, Practical Therapeutics. 
5 Journal American Medical Association. 6 Porter, loc. cit. 

7 Hare, loc. cit. 8 See Dental Cosmos, 1908, p. 185. 



122 DISTURBANCES OF THE VASCULAR SYSTEM 

grains each hour thereafter, increasing to 20 grains, was successfully 
used by C. F. Jones in a ease lasting- several weeks. 1 P. Kinile Weil 
lias suggested the injection of 20 c.c. of fresh human, horse, or rabbit 
serum before operation, for the prevention of hemorrhage in hemo- 
philics, or every three months as a curative measure. 2 Dr. E. W. 
Scott 3 reports the use of 30 c.c. of normal serum by large hypodermic 
syringe as immediately curative of a hemorrhage lasting two and 
a half days after extraction, and 20 c.c. as curative in three to four 
hours in a case of stab wound. Both were blacks. The back was 
selected as the site of injection. To obtain human serum he sug- 
gests a willing volunteer, not a black or relative, a large blister to 
be raised. 

LOCAL DISTURBANCES OF THE CIRCULATION. 

The amount of blood in a part may be increased or diminished. 
The types of local disturbance of the circulation differ as to causes, 
phenomena, and effect, and as to the indicated treatment for each. 

In health the bloodvessels are maintained at a proper caliber 
through the action of two sets of vasomotor nerve fibers : 

1. The vasoconstrictors, which control the involuntary muscles 
of the vessel wall, and which, when stimulated, cause contraction of 
the vessel. 

2. The vasodilators, w 7 hich, when stimulated, inhibit the muscular 
action and permit dilatation. 

Ischemia. — This is local anemia. The quantity of blood in a 
part is less than normal. It is direct when some cause obstructs the 
flow from an artery into a part, as when pressure of any sort is 
applied directly to a part or to the artery leading to it, or when an 
injection of fluid has been made into a part, as in cocain injections. 
Disease of an artery may deprive a part of blood, as in thFombosis 
or arteriosclerosis. Anastomotic circulation may eventually relieve 
a part; if not it remains pale and cold, atrophies, and may undergo 
degeneration or necrosis. An infarct may remain ischemic. 

Arterial Hyperemia. — Arterial or active hyperemia is a more or 
less prolonged increase in the amount of blood in the dilated arteries 
of a part. It expresses the reaction which occurs as the consequence 
of the presence of an irritant, the action of which lessens the arterial 
tension and permits dilatation with a consequent excess of blood. 

Etiology. — The lessened arterial resistance is produced either by a 
stimulation of the vasodilator nerves or a sedation or paralysis of the 

1 New Jersey Dental Journal, October, 1913. 

2 Dental Cosmos, 1908, p. 436. 3 Ibid., January, 1912. 



LOCAL DISTURBANCES OF Till': CIRCULATION 123 

vasoconstrictor nerves. Certain causes act to produce constriction of 
the vessels, hut later the muscle cells of the walls are fatigued and 
dilatation results — e. g., the reaction after the prolonged application 

of cold. 

The removal or diminution of pressure, to which vessels have 
become accustomed, is also a cause of their dilatation; often sudden 
enough to cause bursting. 

Irritants and mild injuries act upon the sensory nerves of a part, 
and by reflex action through the vasomotors (sympathetic system) 
produce hyperemia of the part itself — e. g., heat as a cause. 

Irritation of sensory nerves may induce a reflex hyperemia in other 
parts to which branches of the same nerve are distributed — e. g., the 
peripheral hyperemia of neuralgia, induced by irritation of a tooth 
pulp. 

A similar effect may be produced in deep-seated organs to which 
other nerves are distributed — e. g., hyperemia of deep organs through 
the application of irritants to the skin over them or hyperemia of the 
intestinal wall (tenth nerve) as the result of the stimulation of a pulp 
underlying an erupting tooth (fifth nerve). 

Collateral hyperemia is induced by the diminished flow of blood to 
other parts — e. g., by the bandaging of parts or through the chilling 
of the surface of the body. A part having a lessened resistance may 
become hyperemic. 

Compensatory hyperemia may occur through the removal of one of 
a pair of organs; the other receives the excess of blood, sometimes 
becomes hypertrophied, and takes upon itself an increased amount 
of work. (See Hypertrophy.) A physiological hyperemia occurs in 
organs during periods of activity, the work required acting as a 
stimulus to the vasomotor nerves. 

Arterial hyperemia is produced as the first step in the process of 
inflammation, but can be independent of it. (See Inflammation.) 

Pathology. — The arteries are dilated; there is an increased flow of 
blood through them and also to them through their owm nutritive 
arteries; the pressure in the veins rises as the veins are enlarged to 
accommodate the blood. As exudation sometimes does not increase 
markedly, the lymph pressure is not increased except in marked 
cases, in which some edema may occur. The function of the part 
may be disturbed in the more marked cases. (For illustrations, see 
Hyperemia of the Pulp.) 

Results. — Continued arterial hyperemia, as a rule, results in an 
increase of nutrition, even to the arteries themselves via the vasa 
vasorum. The arteries may be permanently enlarged, their walls 
thickened, and the tissues about them hypertrophied in consequence 



124 DISTURBANCES OF THE VASCULAR SYSTEM 

of the increased capacity for work in the part. Hyperesthesia of 

nerves and nervous tissue is often a result. In marked hyperemia 
with function altered there is a tendency to the degenerations. 
(See Arterial Hyperemia of the Pulp.) 

Symptoms. — These naturally would be and are increased redness, 
temperature, and sensibility; more or less throbbing in marked and 
pathological cases, in some cases swelling and throbbing pain. The 
increased temperature is due to the increased oxidation. (See p. 131.) 

Degrees of Hyperemia. — It is to be borne in mind that the hyper- 
emia may be of several grades, varying from a very mild exaltation 
of function and sensation to a distinctly pathological condition w T ith 
altered function. The effects may be constructive in character or 
destructive, the former due to the increased nutrition, the latter to 
interference with it. (See Constructive and Destructive Diseases of 
the Pulp.) 

Hyperemia as a Resistance to Infection. — -According to Biers and 
others the induction of hyperemia in an infected part increases the 
opsonic power of the excess blood, and therefore is antagonistic of 
infection. No doubt this is the natural process in inflammation. It 
has been occasionally noticed that stimulation, as in the use of a 
capsicum plaster in acute apical abscess, has produced resolution. 
Usually confined abscessses are enlarged and not cured by such 
stimulation. 

Therapeutics. — The principle underlying the treatment is to remove 
the cause and procure surgical rest. The symptoms, as a rule, then 
subside promptly. It may be that the conditions require treatment 
irrespective of the cause, which may not be determined or be absent, 
the vessels being dilated as the effect of a previously acting cause. 
The effect aimed at is the reduction of the dilated vessels. This is 
attempted at times through the use of drugs; for example, ergot 
stimulates the vasoconstrictor system and lessens the caliber of all 
the vessels, including those affected. Aconite, the antagonist of 
ergot, reduces the heart action by sedating the motor apparatus 
of the heart, thus reducing the arterial pressure. 1 Less blood is 
delivered to a part in a given time. Many cases of superficially 
seated hyperemia are amenable to local treatment. 

Local sedation of sensory nerves and contraction of vessels are pro- 
duced by application of dry or w T et cold (ice bags, ice w r rapped in 
muslin, cloths taken in succession from a block of ice, the Leiter 
coil, etc.); also by the application of sedative astringents, as the 
liquor plumbi subacetatis in the well-known formula of lead-water 
and laudanum: 

1 Biddle, Materia Medica and Therapeutics. 



LOCAL DISTURBANCES OF THE CIRCULATION 



125 



1$ — Tincturse opii f5J 

Liq. plumbi subacetatis f5J 

A.qu8B Oj— M. 

in which to the astringent effect of the lead is added the sedative 
effect of the opium; if cold sedation and contraction are added. 

The principle of derivation is also employed. What is known as 
counterirritation is a common means of treatment. An irritant such 
as a mustard plaster or a blister or dry cup applied at a distance to 
the affected part induces a flow of blood to the point of application 
and lessens the amount of blood in the area of hyperemia. The 
volume of the blood being in definite amount, if an excess exists 
in any part a deficiency will be found in other parts. 

The hot pediluvium acts upon this principle by drawing a con- 
siderable excess of blood into the vessels of the lower extremities. 
This action is increased by add- 
ing a small quantity (two or FlG - 59 
three tablespoonfuls) of mustard v ,,4®?f^\ 
to the hot water. It is sug- W^^^^^^^^^ fe^ 
gested by Endelmann that the \(^^iviJ%^^V7^^^s 
water be at first only warm and '"wfiii^At^m) OiH?^ 7 
the hot water added as the ves- »^^^^l^i^W^0~^^^^ 

The volume of the blood may 'j5?^\l. Olf^S^^w^ ^^P^ 
be actually reduced and a deriva- '^J^C ) f\V''«"f^fel^i^^' 

tive hyperemia of the sweat '"' ■ ^^&&\W< 

glands be produced by the use of Tr , , , ,. . m 

j. 'i . ~, . venous hyperemia of the liver. Iwo 

diaphoretics. Cathartics lessen capillaries near central hepatic vein, 
the blood Volume and Cause mild showing the thickening of the walls and 

the accumulation of red blood corpuscles 

hyperemia of the alimentary within them, x 500. (Green.) 
canal. Diuretics act in a similar 

way upon the kidneys. In deep-seated hyperemia counterirritation 
is valuable alone or conjoined with other forms of derivation. 

Venous Hyperemia. — Venous (mechanical or passive) hyperemia 
is an excess of blood in a part beginning in the veins, which are 
dilated in the hyperemic area, though they may be occluded between 
it and the heart. 

Etiology. — 1. Any mechanical interference with the passage of the 
blood through the veins on its way to the heart — e. g., the action of 
bandages, tumors pressing on veins, thrombi in veins, etc. 

2. Insufficiency of any of the mechanical forces aiding the pro- 
pulsion of the blood through the veins— e. g., diminished cardiac 
power or valvular insufficiency; obstructions, dilatations, or rigidity 

1 Dental Cosmos, 1904. 



126 DISTURBANCES OF THE VASCULAR SYSTEM 

of arteries; insufficient muscular contraction upon or valvular 
incompetency in veins, or lessened or excessive thoracic aspira- 
tion, etc. The second class of causes produces a collection of blood 
in the veins and a consequent reduction of volume in the arterial 
system. 

Pathology. — The veins are dilated, the current is slowed, and the 
intravenous pressure is increased, in consequence of which watery 
(serous) exudations occur in the parts about them (edema). For 
the same reason in marked cases diapedesis of red corpuscles may 
occur (hemorrhage by diapedesis), and their hemoglobin may be 
dissolved out. The blood in the parts not being sufficiently changed, 
and in some cases in a state of stasis, there is a lessened food supply 
and waste removal, and cell nutrition suffers accordingly. Vital 
processes are lessened, secretion is diminished, there is less oxidation, 
and hence less heat is produced and less work is done. Fatty degener- 
ation, atrophy, and in markedly continued cases necrosis may occur. 
Long-continued venous hyperemia with great intravenous pressure 
may produce dropsies. If the walls of the veins are weak and 
are permanently distended or thicken under pressure and become 
tortuous, the condition is called varicosity of the veins (varicose 
veins). The exudate of venous hyperemia differs markedly from 
that of inflammation. 1 

Hyperemic Exudate. Inflammatory Exudate. 

Poor in albumin. Rich in albumin. 

Rarely coagulates in the tissue. Usually coagulates in the tissue. 

Contains few cells. Contains numerous cells. 

Low specific gravity. High specific gravity. 

Contains no peptone. Contains peptone (product of cell 

disintegration) . 

This is probably due to an increased permeability in the vessel wall 
in inflammation permitting the albumin of the blood to pass through. 

Therapeutics. — The treatment consists of the removal of the me- 
chanical obstruction to the return of the blood and mechanical sup- 
port of the engorged vessels, with a view to recovery of the tone of 
their muscular walls. This latter is accomplished by means of elastic 
bandages or compresses, and in situations in which these cannot be 
used astringents may be employed. The part is elevated, when 
possible, to aid in the return of the blood to the heart. In certain 
circumstances, as in an engorged tooth pulp, actual depletion of the 
engorged part must be resorted to by bloodletting. (See Destructive 
Diseases of the Pulp.) In cases due to failure of blood-propelling 
forces these are to have appropriate treatment. 

1 Park's Surgery. 



LXFLAMMATION 127 



INFLAMMATION. 



Inflammation may be defined as a series of hyperemic changes 
expressive of the reaction of living tissue to irritation, and character- 
ized chiefly by an excessive diapedesis of leukocytes and exudation 
of coagulable lymph from the bloodvessels. 

Etiology. — Any irritant or injury capable of producing a lesion of 
the bloodvessel wall not involving its immediate death can produce 
inflammation. In case direct death is produced, the inflammation, 
if any, occurs in the tissue contiguous to the dead part. 

The causes of inflammation may be divided first into non-septic 
and septic or infective. The non-septic causes may be extrinsic or 
intrinsic. The extrinsic non-septic causes are: (1) Physical irritants, 
such as violence, mechanical irritation, pressure or traumatism, 
excessive heat or cold, and electrolytic action. (2) Chemical irri- 
tants — e. g., the action of acids, caustics, etc. (3) Nervous or vital 
irritants — e. g., rubefacients, epispastics, arsenic, etc. These act 
only on living tissue through the medium of the nerves. 

An intrinsic non-septic cause may produce inflammation — e. g., 
urates in tissue, mechanical strains upon tissue, temporary lack of 
blood in a vessel or central nervous disturbance, as in herpes from 
locomotor ataxia. 

Xon-septic causes, as a rule, produce only such mild inflammatory 
phenomena as are concerned in circumvallation of an irritant, 
absorption of it, and in repair or production of new tissue. No 
pus is produced unless pyogenic bacteria gain ingress. This class 
of inflammation is termed simple inflammation. 

Septic or Infective Causes. — These are fungi or their products, 
and the classes of inflammations produced are much more severe, 
continuous, and destructive in their nature, and are termed infective 
inflammations. 

Pathology of Simple Inflammation. — If to the web of a frog's foot 
tincture of capsicum be applied, or if its mesentery be exposed to the 
air, and either be examined under the microscope while the animal is 
living, it is noted that after a possible short period of contraction of 
the arterioles dilatation of arteries at once begins and is gradually 
followed by dilatation of the veins and capillaries. This continues 
to steadily increase for about twelve hours. During the first hour 
of this period the blood current is accelerated and the first stage 
of an inflammation is thus an arterial hyperemia. Following this 
acceleration the blood flow is increasingly retarded. The retardation 
is due to the action of the leukocytes, large numbers of the mono- 
nuclear and polymorphonuclear forms of which fall out of the central 



L28 



DISTURBANCES OF THE VASCULAR SYSTEM 



blood stream into the periaxial stream and collect along the walls of 
the small veins (Fig. 60, b). Several layers of leukocytes may thus 
form. Probably some peculiar attraction exists between the leuko- 
cytes and the wall of the vessel, or a positive chemotaxis exists as in 
infective inflammation. 

This massing of leukocytes compels the red corpuscles to the 
centre of the stream (Fig. 60, a), and their passage is mechanically 
interfered with; thus the further dilatation of the vessel becomes 
a process of venous hyperemia. The vessels are increased in size 
and length and become more tortuous. Pulsation is noted. 



Fig. 60 




--■/j 



Small vein in mesentery of dog, after exposure for half an hour and irrigation with 
salt solution : a, red corpuscles; b, leukocytes adhering to wall of vein; c, red corpuscles; 
d, leukocytes which have escaped from vessel; e, leukocyte in act of escaping; /, 
fibrous tissue. X 340. Modified from Thoma. (Green.) 



Coincident with retardation of the blood flow, the leukocytes are 
seen to work their way by an ameboid movement through the walls 
of the veins and to some extent of the capillaries into the perivascular 
spaces — i. e., into the adjoining tissue— in which they may move far 
from their point of escape and mass about the irritant if one be 
present. This process is called emigration (Fig. GO, e). At the same 
time a fluid rich in albumin, and thus capable of coagulation, escapes 
by the same route into the tissue (Fig. 61). Some red corpuscles 
also escape through the walls (diapedesis) (Fig. 60, c). (While 
inflammation involves an arterial hyperemia as its first stage and 



INFLAMMATION VIS) 

a venous hyperemia as its second stage, these two conditions are 
not necessarily inflammation, and may exist as entirely distinct 
conditions when produced by causes not leading to inflammation; 
also, it must he remembered that the results of venous hyperemia 
or infarction, e. (/., extravasation, may lead to a subsequent inflam- 
mation. This does not make them identical.) 

As the venous hyperemia of the inflammation increases, the flow 
of red corpuscles in the veins is increasingly retarded until stopped, 
when a to-and-fro motion (oscillation) begins. Finally all motion 
ceases, diapedesis ceases, and stasis is complete. This blood may 
remain fluid in the vessel for several days (i. e., without coagulation), 
and if the blood flow be reestablished the separate red corpuscles are 
seen one by one to roll away from the general mass until all are in 
movement and stasis ceases. (Thoma.) 

Coagulation (thrombosis) may, however, occur in the vessels 
involved in the stasis, and the part be later removed through the 
process of resorption. (See Resorption of Clot.) With the inflam- 
mation fully established there are in the tissue the following elements : 
(1) Leukocytes and some red corpuscles and lymphocytes from the 
tissue lymphatics. (2) Coagulable lymph. (3) Later new embryonic 
cells formed by mitosis from preexisting connective-tissue cells 
which surround the leukocytes massed about the irritant. These 
are fibroblasts ready to form scar tissue — i. e., they are the elements 
composing granulation tissue. 

The disposition of these elements of inflammation is as follows: 
The leukocytes mass about the irritant, exert a certain amount of 
phagocytic activity (ferment action), 
and may in turn be injured, liberating Fig. 61 

fibrin ferment, which, acting upon the 
fibrinogen of the lymph, produces fibrin, 
which in turn forms a coagulum. This 
coagulum blocks the lymphatic vessels 
leading from the part involved, thus 
causing a retention of fluid in the tissue. 

In the later stages of non-infective in- 
flammation the tissue Cells Undergo multi- Inflammatory edema of skin. 

° . Ine large spaces shown were 

plication, forming cells larger and having filled with exuded fluid, x 
more power of ameboid movement and 2 ' 5 - ( B °y d 
phagocytosis than the leukocytes. These 

become mingled with the leukocytes in the area of inflammation. 
They are fibroblasts from which all the connective tissues develop, 
and to the action of which regeneration is mainly due. Around and 
about the focus of inflammation the bloodvessels are in a condition 
9 K 




130 



DISTURBANCES OF THE VASCULAR SYSTEM 



of arterial hyperemia, and about this is an area of normal tissue. 
These areas shade off into each other. 1 The phagocytes cause disso- 
lution of coagula and dead aseptic tissue, and remove them. If the 
irritant be thus removable it is eaten away. If the dead tissue be 
superficial, the connection with the living tissue beneath is eaten 
through and the latter thrown off. If the superficial tissues have 
been previously removed, the wound is covered with the exudates 
and leukocytes, which dry into a scab, beneath which regeneration 
occurs. If inflammation occur in a mucous surface, the exudate and 



Fig. 62 







Acute bronchial catarrh: Passage of leukocytes through the epithelium of the bronchus 
between the ciliated cells. X 700. (Thoma.) 



corpuscles escape from the submucous tissue between the epithelial 
cells as a catarrhal discharge (Fig. 62) . If the inflammatory exudate 
be highly coagulable and coagulate, firm swelling is caused, apt to 
lead to organization of tissue, hence called fibrinous inflammation. 
If it be productive of hypertrophy, it is called productive inflamma- 
tion. If the exudate be watery, poor in albumin, and hence not 

1 Fig. 64 serves to illustrate these areas, excepting the fact that the central area of 
pus is absent and occupied entirely by an area there termed lesser inflammation — ?'. e., 
translate lesser inflammation into simple inflammation. 



INFLAMMATION 131 

readily coagulable, the inflammation is called serous inflammation. 

In the later stages of simple inflammation the coagula are dissolved, 
the leukocytes undergo fatty degeneration, and both are absorbed, 
together with such tissue as has undergone liquefaction. The lym- 
phocytes and embryonic cells push into the area and regenerate the 
tissue. This is the phenomenon of resolution. 
Symptoms of Simple Inflammation. — These are: 

1. Redness due to the excess of blood in the vessels and in the tissue. 
In some cases the part may have a dusky hue. The color is deepest 
in the area of greatest stasis. 

2. Heat due to the increased oxidation in the area of hyperemia 
about the area of stasis. It has been shown that there is no increased 
heat in the area of stasis. In this area chemical action is lessened. 

3. Sivelling due to the excess of blood in the vessels, the exudates 
of leukocytes and fluid, and the multiplication of tissue cells. The 
hardness of a swelling is due to coagulation of the fluid exudate. 

4. Pain. — The result of the pressure of the effusion upon sensory 
nerve terminals; it is frequently throbbing in correspondence with the 
heart beat; the impulse causes temporarily increased pressure upon 
the nerve terminals. Gravitation also increases the pressure and 
pain in a dependent part — e. g., in a hand or foot or in recumbency 
in case of pulpitis (which see). 

5. Impaired function is an evident result of a disturbance involving 
such pathological phenomena as have been described. The part 
cannot be used owing to pain and stiffness due to the swelling, also 
nutrition of any part being impaired, it loses its normal function. 

There are no general disturbances in simple inflammation beyond a 
slight traumatic fever due to absorption of some aseptic material 
from the seat of inflammation — e. g., fibrin ferment. 1 There may, 
however, be general disturbance due to pain, loss of sleep, appetite, 
etc. Shock due to widespread inflammation, as from burns, may be 
serious. 

Infective Inflammation. — If microorganisms enter the tissue 
through a wound or puncture or an abraded surface, or if they locate 
upon predisposed or non-resistant mucous membrane, their multi- 
plication causes irritation and inflammation of the tissue about them. 
This at first resembles a simple inflammation, but later becomes 
more severe, prolonged, and may spread into the surrounding tissue, 
or in some cases cause inflammation in another place in no way 
connected with it except by the blood or lymphatic channels (metas- 
tasis). Briefly the process may be described as beginning with the 

1 Green's Pathology and Morbid Anatomy. 



132 DISTURBANCES OF THE VASCULAR SYSTEM 

entrance or location of the organisms and their multiplication. An 
injury of the vessel walls and degeneration of some tissue occur 
and the phenomena, such as occur in simple inflammation, begin. 
There is arterial hyperemia, later retardation of the blood current; 
diapedesis of leukocytes occurs, and a copious exudate of coagulable 
lymph is poured out into the intravascular tissue. By positive 
chemotaxis the leukocytes are attracted to the bacteria, surround 
them, and apparently endeavor to limit their activity, or, perhaps, to 
digest them. If the bacteria be few in number and not too virulent, 
the phagocytes are successful and the phenomena of resolution occur. 
If, however, the contrary be the case, the leukocytes are overcome 
and the inflammation spreads. In case of much toxin formation, 
negative chemotaxis occurs and phagocytic phenomena are held in 
abeyance. The central or most involved area dies. It is thus seen 
that there may be two terminations of an infective inflammation — 
resolution and necrosis. 

Resolution. — If the phagocytes destroy or wall up the bacteria, 
so that they die in their own products or are killed by the protective 
juices of the part (alexins), the phagocytes undergo fatty degenera- 
tion, the lymphatics are unblocked, the circulation is reestablished, 
the tissue that has died is removed by resorption and replaced by 
scar tissue if the loss be considerable. No evident pus or externally 
evident necrosis is produced, and the part exhibits phenomena much 
like those of a simple inflammation. This is the only termination 
for a simple (non-infective) inflammation. 

Necrosis. — Death of a part may result from infective inflamma- 
tion, either with or without pus formation. 

Suppuration. — If the irritant in the tissue consists of pyogenic 
organisms, such as the Staphylococcus pyogenes aureus or albus, the 
Streptococcus pyogenes, the Bacillus pyocyaneus, Bacillus typhi 
abdominalis, Bacterium pneumonia?, or the gonococcus, pus will 
be formed, provided the germs be not killed. The Staphylococcus 
pyogenes aureus is most frequently the organism infecting wounds. 
It is practically universal. 

Entering a part, the bacteria distributed in the tissue act as irritants 
and excite the phenomena of inflammation as described. Some of 
the cocci are taken up by the fixed connective-tissue corpuscles, the 
leukocytes, and the endothelial cells of the capillaries, and some lie 
free in the tissue. The cocci multiply and the polymorphonuclear and 
eosinophile leukocytes increase in number by diapedesis and surround 
them. The original tissue cells, including those of the bloodvessels, 
undergo coagulation necrosis as the result of the action of bacterial 
ferments and do not take up staining reagents (Fig. 63). Coagulation 



INFLAMMATION 



133 



of the exudates occurs. The leukocytes and tissue cells arc in part. 
degenerated into pus corpuscles by the action of the unorganized 



fr— 




Miliary abscess in a case of septic embolism of the kidney: a, leukocytes advancing 
toward and surrounding (b) a mass of cocci, in whose neighborhood all trace of struc- 
ture has disappeared; c, renal epithelium too damaged by bacterial products to take 
the stain; d, kidney tissue staining normally; e, vein from which leukocytes are 
making their way to the commencing abscess. X 100. (Green.) 



ferments of the bacteria — i. e., their nuclei are fragmented, and they 
undergo fatty degeneration. Some cocci die. The exudate is pep- 



134 



DISTURBANCES OF THE VASCULAR SYSTEM 



tonized into a fluid, which, together with the cocci, dead leukocytes, 
and tissue remnants, constitutes pus. About this pus is a circum- 
vallating wall of living leukocytes, and about this again a zone of 
fibroblasts arranged about new capillary loops (granulation tissue). 
The whole constitutes, when confined within tissue, an abscess. 
When upon a surface the granulation tissue is upon the under side 
only, the whole constitutes a suppurating ulcer. 






H- 




An abscess in the skin. The horny layer has largely disappeared, and the Malpig- 
hian layer is pushed upward by the subjacent abscess (a). The mass of pus corpuscles 
is just breaking down to form a cavity (P), the walls of which are thickly infiltrated 
with similar cells or the area of stasis (S) . Outside is the area of lesser inflammation 
(LI), and still farther away are the areas of arterial hyperemia (H). and normality 
(N.T). Interpretation modified by editor. (Boyd.) 



While the leukocytes may overcome the bacteria, the reverse is 
often the case, and the pus cavity enlarges in the same manner as at 
first by a new formation of coagulation necrosis, more circumvallation, 
further liquefaction of the coagulum, etc. The path offering the least 
vital or mechanical resistance is usually followed until the surface of 
the body or some internal cavity is reached. The last portion of 
tissue overlying the forming pus is tumefied and a soft, yellow spot 
appears. This is called pointing. The tissue is ruptured by the 
internal pressure and the pus escapes. The tract from the point to the 
abscess cavity is a fistula or sinus. As soon as this occurs granulation 
tissue springs up upon the sides of the abscess cavity and usually 
soon fills it with scar tissue. (See Regeneration.) If the cause con- 
tinues to act, as, for example, in case of a portion of dead and septic 
bone beneath soft tissue, a gangrenous pulp in a tooth root or infected 
crypts of the abscess walls, the granulation tissue breaks down, and 
the condition is one of ulceration or a chronic abscess with a fistula. 
If, in the course of abscess formation, bone be encountered by the 
pus, it may be and often is molecularly broken down into pus. (See 



INFLAMMATION ' 135 

Acute Apical Abscess.) It does not always happen that the pus finds 
escape either naturally or through surgical aid; the patient may die 
before this occurs, or the tissues around the seat of pus formation 
may form a boundary wall which the organisma fail to break down 
and thus die starved out. The abscess contents undergo changes 
resulting in caseation, or later the mass may calcify. In tubercular 
caseations the tubercle bacilli may live for a long period. (See p. 83.) 
The Streptococci pyogenes may multiply laterally, following the 
subcutaneous cellular tissue, and produce violent spreading inflam- 
mation with but little pus formation — e. g., some forms of apical 
abscess and erysipelas. 

The products (toxins) from an abscess or infective inflammation 
may find their way into the blood, and a general toxemia result, or the 
organisms themselves may enter the blood and a general infection 
result (septicemia). There are various varieties of pus which have 
names describing the chief characteristics : 

Creamy pus is the erroneously called laudable pus associated with 
an acute abscess or ulcer which progresses, as a rule, toward a cure. 
It is of a yellowish-white color, creamy consistency, and without 
odor. 

Curdy pus contains flakes. 

Ichorous pus is thin, odorous, and irritating. 

Mucopus is pus containing mucus. 

Seropus is pus containing much serum. 

S anions pus contains blood. 

Cause. — The cause of suppuration is the development in tissues of 
pyogenic organisms. The action of these causes is favored by the 
presence in the part of a hyperemia or simple inflammation, such as 
the injury introducing the organisms may cause. These as well as 
depraved or debilitated tissues favor the action of bacteria — i. e., act 
as predispositions. 

Symptoms. — The symptoms of suppuration are both general and 
local. 

Local Symptoms. — The symptoms of inflammation— redness, heat, 
pain, and swelling — occur, but usually much aggravated. The pain is 
often of a lancinating character, sudden darts often following com- 
parative quiescence. On the other hand, the throbbing pain may 
be continuous and intense, especially when the pus is confined by bone 
or tense tissues, as in the case of a felon or an acute apical abscess. 
Recalling that around the pus area there is an area of stasis, next one 
of active but lesser inflammation, and about that hyperemic, then 
normal tissue (Fig. 64), one may judge of the degree of involvement 
of deeper parts by the appearance of the surface above them. Thus, 



L36 



DISTURBANCES OF THE VASCULAR SYSTEM 



for example, hyperemia at the surface indicates inflammatory action 
directly beneath, with a pus cavity still deeper, while inflammation 
at the surface, together with hardness and tumefaction, shows a more 
involved condition of the tissue directly beneath it- — i. e., a more 
advanced state of inflammation or even of suppuration. 

The softening of the apex of the swelling gives a feeling of lessened 
resistance, indicating pointing or pus at the surface. In large, super- 
ficial abscesses the sensation known as fluctuation may be obtained by 
placing one finger on one side of the swelling and gently tapping upon 
the other. Yellowness of the apex, together w 7 ith softness, indicates 
that the abscess is about to discharge its contents. A fistula or sinus 
upon the surface is indicative of a discharged abscess, and leads to a 
pus-forming area beneath (chronic abscess). 

General Symptoms. — If toxemia be produced there may be chills, 
and, at the same time, fever as high as 104° F. A full, bounding pulse 
accompanies this, the patient is constipated, has a coated tongue, is 
exhausted by loss of sleep and often disturbed nutrition due to the 
pain. There may be other evidences of septic intoxication, wmich 
may become profound. (See Septic Intoxication.) 

Leukocytosis after surgical disease is considered pathognomonic 
of suppuration, the count running up to 15,000 or 20,000 per cubic 
millimeter. (See p. 115.) 

Fig. 65 







Tuberculous ulcer of the intestine: a, mucosa; I, submucosa; c, muscularis; g, ulcer; 
t, tubercle in the mucosa; t', focus caseating in the middle. X 12. 



Ulceration. — The development of microorganisms upon a free 
surface causes tissue degeneration and death, as described under 
Abscess. 

Numerous forms of pathogenic organisms are capable of causing 
tissue degeneration and death of a mucous or skin surface. If infec- 
tion take place through a hair follicle, or if organisms develop upon an 
abrasion, or in the epithelium in conditions of general or local debility, 
the epithelium is destroyed over an area, and in the subepithelial 
tissues the organisms multiply and cause tissue loss. If the organisms 



INFLAMMATION 13"J 

be pyogenic and ulcerous surfaces are usually infected by these 
bodies pus is formed (Fig, 65). Under some conditions, as in 
debilitated and neglected children, the ulcerous process may spread 
rapidly, as in the cheek in caneruni oris; or when specific bacilli, 
which excite much swelling- and quick death of the tissues of the 
cheek, proliferate, causing the condition called noma. (See Index.) 

Prognosis. — Abscesses tend, as a rule, to spontaneous cure without 
marked systemic disturbance. If the pus discharge persist after 
evacuation of the abscess, persistence of the cause, or infection of the 
abscess w r alls through reinfection or by retention of bacteria in the 
crypts, is to be suspected. The recurrence of rigors (chills) and high 
fever is a danger signal. A fluttering, weak pulse and clammy extrem- 
ities indicate profound septic intoxication, and are indications for 
local disinfection and systemic treatment. 

Therapeutics of Inflammation. — If the cause of inflammation be in 
evidence it must be removed ; good examples of removable causes are 
a splinter in the flesh, a gangrenous tooth pulp, etc. Ordinarily the 
pus of an abscess or an ulcer contains the cause (bacteria) within it; 
therefore the pus should be removed by opening the abscess, if its 
situation can be determined, after which the pus cavity is syringed out 
with germicides, which destroy the pus and the organisms. Hydrogen 
dioxid in 3 per cent, aqueous solution is commonly used; it is made 
more effective by the addition of mercuric chlorid (1 to 1000). 

In ulceration the pus and organisms are destroyed in a similar 
manner, though at times sloughing tissue requires removal by the 
curette, caustic agents, or by digesting agents, as caroid, papoid, 
brewers' yeast, 1 etc. 

Dead bone acts as a septic irritant and requires removal, and at 
times an abscess will remain persistently infected, requiring surgical 
removal of tissue. The abscess or ulcer, if protected from further 
infection, usually heals by formation of granulation tissue. A deeply 
seated abscess may require to be packed with antiseptic gauze (noso- 
phen), in order that it may granulate from the bottom out; otherwise 
a small orifice may heal, permitting a re-collection of pus beneath. 

Ulcers are usually dusted with antiseptic powders, iodoform, aristol, 
or nosophen, which cause drying of the surface and prevent the access 
or action of organisms. Under certain circumstances the presence of 
suppuration is not certain, though phlegmonous (spreading) inflam- 
mation is somewhat pathognomonic of it. In such cases hot, moist 
applications, such as hot poultices, soften the surface above the 
abscess and determine its direction of discharge, thus limiting burrow- 

1 Park's Surgery. 



138 DISTURBANCES OF THE VASCULAR SYSTEM 

in»-. Counterirritants applied directly above the inflamed area also 
hasten in such cases. The stimulation may aid resorption (destruc- 
tion by phagocytosis) of the pus and resolution occur. 1 The vascular 
engorgement in an inflamed part may be reduced by local bloodletting. 

Nancrede found, on dividing a vein upon the distal side of an area 
of inflammation, that after a brief period the flow of blood was 
established through the inflamed area. Local bloodletting by 
leeches (Gensmer) produced even more marked effects. Drugs which 
stimulate the vasoconstrictors (ergot), and those which paralyze the 
constrictors (aconite), lessen the blood pressure in the inflamed area; 
so that if administered in the early stages of inflammation they may 
modify its severity. If, on the contrary, they are administered after 
stasis occurs, they increase the stasis — ergot actively and aconite 
passively. If the flow of blood through the inflamed area be reestab- 
lished by local bloodletting, then the arterial sedatives are distinctly 
useful in lessening the flow of blood to the part. 

When, owing to vascular engorgement, throbbing pain is a promi- 
nent symptom, applications of cold are useful in lessening the caliber 
of vessels and in relieving pain. But if there be firm exudation and 
marked stasis, cold is a detriment. Heat then gives relief through 
inducing a more free flow of blood in the collateral circulation. Very 
hot applications act as do cold applications, by causing contraction of 
vessels, and may be used to abort an inflammation. 

In certain situations, as in case of an inflamed tooth-pulp, sedative 
applications, antiphlogistics, are required. Conjoined with local 
measures of reducing vascular engorgement, the use of counter- 
irritants and general derivatives are indicated. (See Treatment of 
Hyperemia.) 

General sedatives are at times demanded for the relief of pain. 
Morphin used in small and continued doses not only relieves pain, 
but causes a contraction of small vessels. Other anodynes are also 
used in this connection, as acetanilid or trigemin. Quinin and salol 
are useful as correctives of the intestinal disturbance, and mercuric 
chlorid in small doses is useful as a preventive of general infection. 
(See Acute Apical Abscess.) 

REGENERATION OF TISSUES. 

Connective tissues that have been lost by inflammatory process or 
operation are replaced by granulation tissue arising by mitotic division 
of cells of the connective-tissue group. The forms of healing are by 

1 Park's Surgery. 



RHGKXKRAriOX OF TISSUES 



39 



first intention, second intention or granulation, healing under a seal), 
and healing under a clot. Epithelial tissues are replaced only by 

Fig. 66 




Regeneration of capillary bloodvessels: a, normal capillaries; b, capillary process; 
r, now capillary appearing in divided process; d, process undergoing division; e, con- 
necting cell in which no sign of division has yet appeared. Diagrammatic. (Green.) 



Fig. 67 



© <3 © O 
© o © c^© 




A granulating surface: a, layer of pus; b, granulation tissue with loops of blood- 
vessels; c, commencing development of the granulation tissue into a fibrillated struc- 
ture. X 200. Diagrammatic. (Rindneisch.) 



140 



DISTURBAXCES OF THE VASCCLAK SYSTEM 



multiplication of epithelial cells. The forms of healing arc practically 
alike by formation of granulation tissue, the form being simply a 
modification (of extent) of healing by second intention. This granu- 
lative tissue is transformed into fibrous tissue, the original tissue 
rarely being reproduced to any great extent though bone may be 
regenerated. 




Transverse section of granulation tissue from an open wound with fibropurulent 
deposit: a, granulation tissue; b, fibropurulent deposit; c, c, bloodvessels. X 150. 
(Ziegler.) 



Healing by Second Intention or Granulation. — Shortly after evacu- 
ation of pus from an abscess the process of repair is instituted. The 
leukocytes come to the surface of the wound in great numbers; some 
of these may degenerate into pus cells. Immediately beneath the 
uninjured connective-tissue cells multiply, forming embryonic cells 
(fibroblasts) ; at the same time the endothelial cells of the capillaries 
multiply at points, throwing out solid-pointed projections or buds 



RKCKXKhWTIOX OF T/SSCluS 



141 



from the sides of the capillaries (Fig. 66, b). These lengthen and 
join buds from other capillaries (Fig. 66, c, d, e). By mitosis the 
nuclei divide horizontally, lying side by side (Fig. 66, d). Later these 
separate into two cells, discovering a lumen into which blood enters 
from the parent capillary (Fig. 66, a', c). In this manner loops are 
formed, about which the fibroblasts are arranged (Figs. 67 and 68). 

Together these form minute red elevations upon the surface of the 
abscess cavity or wound, called granulations. Repeated, the process 



gradually fills the abscess cavity. 



Fig. 69 




Laparotomy wound — sixteenth day: a, a, epithelium; b, b, corium; c, subcutaneous 
fat; d, vessels in scar tissue of corium; e, newly formed epithelial layer; /, vessels in 
subcutaneous scar tissue. X 40. Modified from Ziegler. (Green.) 



Naturally, collapse of the walls or apposition of cut edges of a 
wound lessens the amount of granulation tissue necessary; hence, in 
the latter case, healing by first intention (with a minimum amount 
of granulation or scar tissue). 

The wound having been filled up, epithelium grow r s from the sides 
and covers the granulations (Fig. 69, e). The granulation tissue, at 
first highly vascular, later contracts, and many vessels are obliter- 
ated so that it becomes wdiiter than normal tissue — cicatricial tissue 
(cicatrix). 



142 



DISTURBANCES OF THE VASCULAR SYSTEM 



Fig. 70 




The indifferent embryonic cells may have the function of forming 
any of the connective tissues. If cartilage is to be formed, chondrifi- 
cation takes place about the specialized cells. If bone is to be formed, 
certain cells form islets, about which calcification proceeds. Nerves 
require a month or more to pierce the cicatricial tissue (Eichhorst). 1 
In spite of this assertion the writer finds that granulations are very 
sensitive to touch, which seems clinical evidence of error in this 
observation. 

In healing beneath a scab the exudation and leukocytes upon the 
surface of the wound dry into a scab beneath which granulations 

and an epithelial covering are 
formed. Later the scab falls 
off. If prematurely lost the 
granulations are exposed. 

In healing under a clot the 
clot is invaded by leukocytes, 
which have a solvent action 
upon it. Granulation tissue 
forms upon all sides of it, 
grows into it, and, at the same 
time, removes it by resorption 
(Fig. 70). If the clot become 
septic the granulations may be- 
come infected and break down, 
as scar tissue in its early vas- 
cular stages is of but feeble 
resistive power, though it does 
not absorb toxins. (Park.) 

Healing under a clot is the 
form commonly seen after 
tooth extraction. It is an in- 
teresting point that the alveo- 
lus is finally filled with bone, 
while the original bony margins 
of the alveolus are resorbed. 

In certain cases of abscess 
with contracted fistula? or open- 
ings of discharge, the orifice may close before the granulations have 
filled the pus cavity. If pus or an excess of exudate be now formed 
within the cavity, a second discharge may occur. To obviate this diffi- 
culty, abscesses are often packed with antiseptic gauze, so that healing 




- i 




Absorption of blood clot. Section through 
the margin of a clot formed among the tissues 
by extravasation, showing the growth of 
granulations by which it is removed: a, a, 
portions of clot; b, b, original tissue; c, c, 
granulations springing from the original tis- 
sue and projecting into the clot; d, d, wan- 
dering cells or leukocytes that seem to have 
taken red blood disks into their interior. 
(Section cut in gum arabic and stained with 
hematoxylin.) X 350. (Black.) 



Ziegler, General Pathology 



INFLAMMATION OF BONE I L3 

may occur from the bottom of the cavity, while drainage is assured. In 
other cases the placing of a tent or drain tube in the fistula together 
with asepsis suffice for the attainment of the object. In other cases, 
as in bone cavities, semisolid materials, such as Beck's bone paste 
are introduced to occupy the cavity to exclude infective and foreign 
material while granulations form about it and gradually absorb it. 

INFLAMMATION OF BONE. 

"Active inflammatory changes may occur in the periosteum, the 
medullary canal, the medullary spaces of the spongy bone, and 
the Haversian canals, the compact tissue and ground substance 
remaining passive." 1 The inflammation is termed periostitis, osteo- 
myelitis, or osteitis, the terms referring to the point of location of 
the inflammation — i. e., the periosteum, the medulla, and the spaces 
— the bone being involved in all cases. Inflammation of bone may 
be non-infective or infective; the latter is usually due to pyogenic 
organisms — i. e., suppuration occurs. 

Proliferative Periostitis. — This is a proliferation of cells of the 
deeper layers of the periosteum combined with emigrated leukocytes. 
A node is thus formed which may ossify. 

Suppurative Periostitis. — Pyogenic organisms may enter an 
injured periosteum or one weakened by previous disease (e. g., by 
scarlet fever). The origin of the bacteria is by way of the blood, 
either directly or by way of the medulla (as a secondary effect of 
osteomyelitis), or by way of the skin. 

Pus forms beneath the periosteum, raises it, and destroys its 
connection with the bone. The vessels are stretched, damaged, and 
thrombosis occurs. Superficial necrosis of bone results, which may 
be total if other sources of blood supply are also cut off. 

Acute Osteomyelitis. — This is a suppuration occurring in the 
bone-marrow, which infects the bone proper, causes much throm- 
bosis of vessels, coagulation necrosis of bone cells, and may rapidly 
cause much necrosis of medullary tissue. Occurring in large bones, 
much toxin is produced, which may rapidly cause death. The organ- 
isms and thrombi formed, becoming emboli, may rapidly lead to 
pyemia. 2 Prompt surgical interference is called for. 

Inflammation of bone may lead to its rarefaction (rarefying 
osteitis or osteoporosis), its condensation (condensing osteitis or 
osteosclerosis), or its death (necrosis and caries). 

1 Schmaus and Ewing, Pathology and Pathological Anatomy. 

2 Park's Surgery. 



144 



DISTURBANCES OF THE VASCULAR SYSTEM 




/.'•"' - i * ' 



■>?*■■£ 



Rarefying Osteitis (Osteoporosis). — In the rarefying process 
which occurs in chronic inflammation, granulation tissue is formed, 
which enters the Haversian canals and spaces of spongy bone and 

destroys (resorbs) the bone, owing 
to the presence of osteoclasts. They 
thus form new channels between 
the spaces — perforating canal re- 
sorption (Fig. 71). With suppura- 
tion (ulceration) added, the granu- 
lations break down, leaving the 
bone as a dead, spongy, or honey- 
combed mass. This is caries of bone. 
In the early stages the inflamma- 
tion may cease, and the bone not 
only be restored, but condensed. 
Condensing Osteitis (Osteosclerosis). — In chronic inflammation, 
of lesser degree, instead of rarefaction, construction occurs and the 
trabecule of bone may increase in thickness, so that all spaces and 



v. - - - - „ - ,. 




yJ'^ : -_ A' '■''*'*, ''-'V% 



Trabecular of bone with perforating 
canals. X 50. 



Fig. 72 



Fig. 73 





Section of bone and periosteum cover- 
ing it: B, bone; c, outer fibrous layer; 
a, inner layer of white fibrous tissue; O, 
layer of osteoblasts, some of which reach 
the bone with their prolongations. Nor- 
mal bone. (Black.) 



Section of bone and periosteum 
covering it: a, osteoclasts, cells that 
absorb bone; b, surface of bone, 
showing fibers of periosteum pene- 
trating it and a Howship lacuna. 
Lacunar resorption. (Black.) 



Haversian canals become smaller. The bone becomes very compact 
and less vascular, and if built up in excess of its original dimensions, 
constitutes the condition known as exostosis; if very dense, as " ivory 



INFLAMMATION OF BONE 



145 



Fig. 74 






exostosis." Both condensing and rarefying osteitis occur about the 
alveolar process and the roots of teeth. (See Hypercementosis 
and Resorption.) 

Necrosis of Bone. — Necrosis 
of bone following rarefying 
osteitis is known as caries. 
It is a molecular death of 
bone. Subperiosteal death of 
bone occurs from infective 
periostitis, and is due to the 
compression of vessels by the 
exudation and to thrombosis. 
Nutrition ceases; death results. 
The dead piece is demarked 
by a line of leukocytes (phago- 
cytes), solution of continuity 

or rarefying osteitis occurs at the line of union with the living 
bone, and the piece is thrown out as a sequestrum. New bone 




Lattice-work figures in halisteresis. 
v. Recklinghausen.) 



(After 




Fig. 76 



9 & 



c~< 



fcSK& 



<"*% 



:v A. 



: -:vv v 



M 



Diagram of healing frac- 
ture. From a guinea-pig 
ten days after injury: K, 
ends of the bone: m, mar- 
row; c, periosteal callus; 
d, « medullary callus; o. 
osteoid tissue. X 6. 



The same preparation: M, myelogenous callus; 
P, periosteal callus; K, ends of the bone; k, osteoid 
trabeculae; o, osteoblasts in rows; p, thickened 
periosteum. X 250. (Schmaus and Ewing.) 



inclosing a sequestrum is termed an involucrum. (See Gan- 
grene.) 
10 



146 DISTURBANCES OF THE VASCULAR SYSTEM 

Resorption of Bone. — Under conditions of chronic inflamma- 
tion bone is often removed by neighboring tissue in one of several 
ways. 

Lacunar Resorption. — In this form the bone is excavated by giant 
cells into bays called Howship's lacunse, which may enlarge, or later 
a reconstructive action may occur and osteoblasts may fill up the 
bays with bone. (See Hypercementosis and Resorption of Roots.) 

Perforating Canal Resorption. — This has been described under 
Osteoporosis. The canals connecting medullary spaces are enlarged 
by the granulation tissue formed in them (Fig. 71). 

Halisteresis Ossium. — In this form of resorption the bone first 
undergoes decalcification and the matrix is later removed (Fig. 74). 
It occurs in conditions of osteomalacia, as in pregnancy, senility, 
etc. It also occurs in the alveolar process, and is, at least in part, 
the cause of the cleanly symmetrical resorption of the gum and 
alveolar margins. (Talbot. 1 ) 

Regeneration of Bone. — Bone lost by suppuration is first replaced 
by provisional tissue of the connective-tissue type, in which appear 
osteoblasts. Calcification then proceeds under superintendence of 
these (Figs. 72, 75, and 76). 

FEVER. 

The term fever is applied to a condition the most prominent 
feature of which is an elevation of the bodily temperature above 
the normal, 37° C. To constitute a fever this rise in temperature 
must continue for some length of time. 

Etiology.— Fevers are commonly caused by the presence in the circu- 
latory fluids of substances which act as poisons upon, probably, the 
nerve centres controlling heat production. As a rule, the offending 
substance is a poison generated in the body through the action of 
microorganisms. The character and type of the fever are deter- 
mined by the nature of the offending substances — i. e., the variety 
of infection. 

Classes. — Fevers are divided into periodical or continued, according 
as to whether there is a periodical fall of temperature and a subsequent 
rise, or whether the fever continues practically unabated from the 
beginning to the termination of a disease. Fevers are classed in 
severity according to the maximum temperature, and, again, accord- 
ing to their duration. A temperature of 100.5° to 101.3° F. is called 
slightly febrile; 101.3° to 103° F., moderate fever; 103° to 105° R 
marked fever. A temperature above 106° F. is termed hyperpyrexia t 

1 Interstitial Gingivitis, 



FEVER 147 

Symptoms. — The most characteristic symptom of fever is the eleva- 
tion of temperature; accompanying this there is an increased fre- 
quency of the pulse. In acute inflammatory diseases the pulse is full 
and bounding, the eyes injected, the bowels constipated, and the 
urine scanty, containing an excess of urea. On standing, the urine 
throws down a brickdust deposit (urates). In fevers of a lower type, 
or in many fevers which begin as described, the high, bounding pulse 
is succeeded by a soft, quick pulse, and evidences of great debility. 
In fevers in which the temperature runs high there is commonly 
evidence of intoxication, more or less delirium, and reflex muscular 
action. With a persistent temperature and a pulse becoming softer 
and more frequent, there is increasing debility. 

Pathology and Morbid Anatomy. — In all cases of continued high 
temperature the fat of the body rapidly disappears and granular 
degeneration occurs in the muscles and viscera of the body. If the 
fever be long continued and of an adynamic type, this degeneration 
may become marked. Its occurrence in the muscles of the heart is 
common and is an element of danger. There are an increase in the 
amount of carbon dioxid formed and exhaled from the body, and 
an increased amount of oxygen inhaled. This, with the increase of 
urea, the product of the oxidation of nitrogenous tissues (muscles, 
glands, etc.), indicates that the oxidation of the tissues is largely 
increased; hence the elevation of temperature. As repair does not 
equal waste in fevers, the nutritive processes being profoundly dis- 
turbed, the essential elements of the tissues suffer from the increased 
oxidation and undergo degenerative changes. 

Prognosis. — The higher the temperature and the longer it continues, 
the greater drain there is upon the vital forces. As a rule, a tempera- 
ture of 106° F. persisting more than twenty-four hours presages 
death. If the vital forces flag and the heart action becomes weakened, 
and if there be evidence of profound intoxication, such as twitching 
of tendons, low, muttering delirium, and a clammy surface, the out- 
look is bad. Favorable signs are: falling temperature, a clear eye, 
tongue losing its coating, free action of the bowels, free perspiration, 
free action of the kidneys, and a good vascular tension. 

Treatment. — In the light of present knowledge efforts should first 
be made to discover the nature of the cause of the fever and to remove 
it, if possible. If not, attention should be directed to maintaining the 
vital forces until the body rids itself of the offending causes. As 
many fevers are self-limited in course and duration, this latter treat- 
ment becomes an important consideration. The temperature should 
be kept within safe limits by the administration of antipyretics, 
when the condition of the heart will permit their use, and also by 



148 DISTURBANCES OF THE VASCULAR SYSTEM 

cool sponging or cool baths. The action of the heart should be 
sustained by the administration of concentrated nutriment, and by 
stimulants when necessary. The bowels must be kept open. 

In any form of fever there is no therapeutic measure comparable 
with the removal of the cause, provided this be discoverable, iden- 
tified, and removable. 

TOXEMIA. 

By toxemia is meant a more or less general disturbance of the 
ecomony as the result of the presence in the blood of substances 
poisonous to a tissue or the tissues. The substance may be a normal 
constituent of the blood which has accumulated owing to faulty 
elimination — e. g., urea — or be derived from the alimentary canal as 
the result of unusual fermentation therein. Such an effect is known 
as auto-intoxication. It may be due to the action of drugs of toxic 
character — e. g., alcohol or iodoform. This is drug toxemia. Again, 
it may be due to the action of the products of bacteria, which prod- 
ucts, absorbed from certain foci of infection, produce general effects, 
such as fever. Again, similar results can be produced by the intro- 
duction of toxic products from bacterial culture in vitro or in experi- 
mental animals. 

Septic Intoxication. — By septic intoxication is meant the absorp- 
tion into the blood of the products of bacterial activity, which 
products are produced at some focus or foci of infection as the result 
of tissue or tissue-juice decomposition. These bacterial products 
produce symptoms of general poisoning or intoxication, which are 
mild or severe, according to the character of the poisonous body 
produced. The organisms do not necessarily enter the blood, hence 
the blood is not infectious if inoculated into another person (or 
experimental animal). 

Two varieties of septic intoxication may be distinguished: 

1. Intoxication by the products of the action of specific bacteria 
developing upon living tissue. 

2. Intoxication by the action of bacteria upon non- vital materials 
(sapremia). 

The action of the bacilli of diphtheria, Asiatic cholera, and tetanus 
are examples of the first class. Their toxins are virulent, but the 
bacteria are confined to the pharynx, intestine, and the wound 
respectively. 

Sapremia. — The entrance of putrefactive or the pyogenic organ- 
isms into such material as a large blood clot or gangrenous area may, 
by putrefaction, cause the formation of large quantities of toxins. 
These, if absorbed, produce rapid and profound symptoms of intoxi- 



SEPTICEMIA 149 

cation. The symptoms vary according to the nature of the toxin and 
the quantity absorbed, but ordinarily occur in the following order: 
Malaise, rigor, fever and its symptoms, nausea, vomiting, headache, 
diarrhea, prostration, delirium in some cases, muscular weakness, 
clammy skin, feeble pulse, quick respiration, and in fatal cases coma 
and death. The symptoms are similar to those of septicemia, but 
appear more rapidly — i. e., septicemia requires time to spread. There 
is a putrid wound which is the source of the toxic substance. The 
condition is usually complicated by septicemia. 

SEPTICEMIA (GENERAL SEPTIC INFECTION). 

By septicemia is meant a condition in which the bacteria, usually 
one of the pyogenic varieties, gain entrance to the living tissues, 
enter the circulation, and are carried to inaccessible parts, where 
their development continues and from which point their toxins are 
absorbed (Fig. 77). 

This process requiring more time than mere absorption of toxins, 
the symptoms are much more delayed than in sapremia. The blood 
is highly infective to susceptible animals in minute amount, as it 
contains bacteria. 

Pathology. — There is a septic wound in which incubation occurs for 
several days. The lymphatics leading from the part and the nearest 
lymphatic glands become inflamed. In pronounced cases the spleen 
is enlarged. There is marked leukocytosis. 

Examination made after death due to the septic intoxication 
produced by both sapremia and septicemia exhibits fairly constantly 
enlargement of the spleen and disintegration of the red corpuscles, 
with staining of the intima of the vessels and heart. The lungs are 
congested. Death occurs through heart-failure. 1 

Symptoms. — These are similar to those of sapremia, except that the 
periods of incubation about the body cause delays. 

Therapeutics. — For sapremia and septicemia, the treatment is both 
local and general. The local treatment involves the opening and dis- 
infection of all wounds, even the extirpation of a part and of neighbor- 
ing glands being sometimes necessary for removal of the cause. If 
possible, the part is immersed frequently r in hot water, which may 
occasionally have mercuric chlorid added to it. 

An antiseptic salve, consisting of resorcin, 5 parts; ichthyol, 10 
parts; unguentum hydrargyri, 40 parts; lanolin, 45 parts, is to be 
applied to the area of infection. 2 

1 Green, Pathology and Morbid Anatomy. 2 Park's Surgery. 



150 



DISTURBANCES OF THE VASCULAR SYSTEM 



Crede's silver ointment may be applied to the unbroken skin for 
the systemic antiseptic effect of the silver. 

The general treatment consists in: (1) Clearing the alimentary 
canal by means of cathartics and maintaining its asepsis by means 
of mercuric chlorid in small doses, salol, or other suitable antiseptic. 

(2) Supporting the heart action by means of alcohol and strychnin. 

(3) Supporting the strength by concentrated liquid nourishment, such 
as egg albumen, beef peptonoids, beef juice, peptonized milk, 1 to 



Fig. 77 







Pectoral muscle beset with large numbers of the Streptococcus pyogenes, from a 
case of phlegmonous inflammation of the subcutaneous and intermuscular connective 
tissue, due to cadaveric poisoning (the phlegmon of the wall of the chest developed 
two days after the finger was injured, and the intermediate lymph vessels of the arm 
showed no evidences of being involved) : a, perimysium internum full of streptococci ; 
b, transversely cut muscular fibers, still intact; c, transversely cut muscular fibers 
which are beginning to degenerate; d, muscular fibers into which the cocci have pene- 
trated. (Preparation treated with gentian violet and vesuvin, and mounted in Canada 
balsam. X 350 diameters.) (Ziegler.) 



which diet fruit may be added. 2 (4) Reducing the temperature by 
means of cold sponge baths or quinin. (5) Maintaining the elimina- 
tive action of the kidneys until the system has rid itself of the toxins. 
For the more profound cases, Park recommends the intravenous 
infusion, as an intravascular germicide, of from 500 c.c. to 1000 c.c. 
of a solution of Crede's soluble silver, 1 to 1000 of sterilized water 
at 105° F. Streptococcus antitoxin is sometimes used. Vaccine 
therapy is of value. (See p. 63.) 



Thompson, Practical Medicine. 



2 Park's Surgery. 



PYEMIA 151 



PYEMIA. 



By pyemia is meant a form of septicemia or septic infection by 
pyogenic organisms, which, locating at favorable spots, as in the 
capillaries, multiply and produce numerous abscesses known as 
miliary or metastatic abscesses. From these foci toxins are absorbed, 
which produce a septic intoxication. 

The organisms may enter the blood from some focus of suppuration 
as free cells or be taken up by leukocytes, or thrombosis may occur at 
the original focus of infection, and portions of clot be carried in the 
blood as septic emboli to terminal arteries, where the results of septic 
infarction are set up. (See Infarction.) 

Symptoms. — The symptoms of pyemia are, in general, those of 
septicemia; their appearance is delayed from the date of the reception 
of an injury or the outbreak of the primary suppuration. The onset 
of pyemia is usually by a chill or a succession of chills. Each fresh 
area of pus formation is believed to be announced by a chill and a 
rise of temperature. The temperature is subject to remissions, and 
sudden variations in its height are noted. The general symptoms are 
those of an adynamic fever. Local symptoms appear according to 
the point of lodgment of septic emboli. Pus centres may be found 
in the lungs, and cause symptoms of dyspnea; collections frequently 
occur in joints, causing loss of mobility; eruptions appear on the skin, 
the swellings being apparent; typhoid symptoms become more pro- 
nounced, and an increasing debility ushers in a usually fatal ending. 
At times both septicemia and pyemia may become chronic. 

Therapeutics. — The treatment of pyemia should be preventive. 
The carrying out of rigid antiseptic precautions has much lessened 
the frequency of pyemia. If areas of infection are removable, they 
are removed no matter what extent of operation may be necessary. 
The general treatment is the same as in septicemia, with much less 
hope of recovery. 

A consideration of the infective surgical processes in connection 
with dental and oral diseases is of the utmost moment to the prac- 
titioner of dentistry. Nearly T all of the diseases which the dentist is 
called upon to treat are infective from their inception. Moreover, 
the saliva, holding in suspension numerous forms of bacteria, both 
saprophytic and parasitic, and their waste, is a highly infective fluid. 

It has been clearly demonstrated by the researches of Miller 1 that 
many forms of bacteria found in specific diseases, and found inhabit- 
ing the intestinal tract, are more or less constantly present in the 

1 Microorganisms of the Human Mouth. 



152 DISTURBANCES OF THE VASCULAR SYSTEM 

human mouth, and that the pathway in many genera] infections is 
no doubt via the oral cavity. A wound made in the human mouth is 
necessarily an infected wound. In the vast majority of cases the 
body exercises its protective function in a phagocytosis, 1 or through 
immunizing processes, which disposes of invading bacteria or renders 
them innocuous. In other cases it is beyond question that this 
protective provision fails and infection occurs, especially if new forms 
be introduced. 

THE EXANTHEMATA. 

Certain acute specific diseases, such as rubeola, rotheln, scarlatina, 
varicella, and variola are accompanied by skin eruptions generally 
distributed over the body, and which represent an infective derma- 
titis; indeed, the eruptions of many of these diseases are contagious 
to other individuals. Syphilis, a chronic specific disease, due to the 
Treponema pallidum, produces similar effects. 

The special interest lying in the exanthemata is that occurring 
during the development of the teeth; the latter are often profoundly 
affected, so that malformations, sometimes serious in character, occur 
in the teeth. It is to be recalled that teeth are dermoid structures, 
certainly in so far as the enamel is concerned. (See Malformations 
of the Teeth.) Again, after or during exanthematous diseases, 
notably scarlet fever, the oral tissues are much debilitated, so that 
abscesses about the teeth may produce much necrotic tissue or the 
disease itself may produce necrosis. 

1 Hugenschmidt, Dental Cosmos, 1896. 



SECTION II. 

EMBRYOLOGY, ANATOMY, AND HISTOLOGY. 



Fig 



CHAPTER VI. 

THE DEVELOPMENT, ANATOMY, AND HISTOLOGY 
OF THE JAWS AND TEETH. 

As malformations of the parts about the mouth and of the teeth 
are dependent upon defective development of the same, it is incum- 
bent that certain facts concern- 
ing their embryolog} 7 should be 
stated. In like manner, as the 
processes of pathology are modi- 
fied by the peculiar anatomy of 
the teeth and associated parts, 
it is necessary that a previous 
knowledge of these be acquired 
before the special dental path- 
ology can be comprehended. 
The embryology of the mouth 
begins at a very early period — 
before the twelfth day the future 
mouth may be located (His, 
Fig. 78). The mouth and 
nasal cavity are circumscribed 
by parts which are developed by 
outgrowths from the head fold 
of the fetus. Those structures 
immediately concerned are the 
lateral tubercles arisi 
the frontal prominence (Fig 




twenty- 



Face of an embryo of 
twenty-eight days (magnified fifteen times) : 
1, frontal prominence; 2, 3, right and left 
from olfactory fossae; 4, inferior maxillary tu- 
bercles, united in the middle line; 5, superior 
maxillary tubercles; 6, mouth or fauces; 7, 



79), which grow downward and second pharyngeal arch; 8, third; 9, fourth; 
fuse, forming the nose, the 10 primitive ocular vesicle; 11, primitive 
' ° \ auditory vesicle. (Gray.) 

nasal septum, the intermaxillary 

bones, and anterior portion of the upper lip (Figs. 80 and 81). From 

the sides of the head fold at the level of the mouth and neck appear 

(153) * 



Ill ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 

certain lateral protuberances, or pharyngeal arches. The first 
pharyngeal arches (Fig. 78, 4) divide into (1) the superior maxil- 

Fig. 79 



Sup. tubercle 
Lateral tubercle 




Sup. tubercle 
Lateral tubercle 



Head of an early human embryo, showing the disposition of the facial fissures and 
the superior and lateral tubercles. (His.) 



S.M.P; 




S.M.P. 



NAS. 



Diagram illustrating scheme of union of the processes: N.S., lateral tubercles 
forming internal maxillary bones, INT. MAX., and nasal septum; S.M.P., superior 
maxillary processes forming palatal processes of superior maxillae, S.M.P.; N.C., 
nasal cavity; O.C., oral cavity; I.M., inferior maxillary processes united. 



lary processes (Fig. 78, 5) and (2) the inferior maxillary processes 
(Fig. 78, 4, shown just beneath the oral cavity and united in the 
median line). 



lie:. 81 




Complete bilateral fissures (coloboma) of face. (Guersant.) 
Fig. 82 



\ 




* Vertical transverse section through head of human embryo, about the tenth week: 
1, nasal cartilage; 2, buccal cavity; 3, tongue; 4, dental ridge, lower jaw; 5, nasal 
cavity; 6, dental ridge, upper jaw; 7, dental ridge, lower jaw. X 30. (Broomell. 1 ) 



Anatomy and Histology of the Mouth and Teeth. 



156 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 

The superior maxillary processes develop the palate hones and the 
superior maxilla'. They form the balance of the upper lip. The 
arch itself forms the cheek. Fig 81, from a ease of arrested develop- 
ment, illustrates the unions and parts naturally formed, hut here 
incomplete. Fig. 82, in which the union of the processes is still 
incomplete, shows how this and cleft palate can occur. 

Secondary processes develop horizontally toward each other, form 
the palatal portions of the superior maxillae and palate bones, and 
unite at the median line (Fig. 80, S.M.P., also Fig. 82), forming the 
vault of the mouth and floor of the nasal cavity. Union occurs with 
the lateral processes, later forming the intermaxillary bones and bear- 
ing the germs of the incisor teeth (Fig. 83), thus completing the 
formation of the upper jaw and lip. 



Fig. 83 



One for nasal and 
facial portions. 



One for orbital and 
malar portions. 




A titer ior Surface. 



At birth. 



One for incisive 
portion. 



One for palatal 
portion. 




Inferior Surface. 

Development of the superior maxillary bone by four centres, also development of 
intermaxillary bones. (Gray. 1 ) 

The inferior maxillary processes grow forward and unite at the 
median line, developing the inferior jaw and lip. Fig. 86, an arrested 
case, shows this. 

The structures of the floor of the mouth and neighboring structures 
are formed from the second, third, and fourth pharyngeal arches and 
a tubercle arising near the first pharyngeal arch. The fusions of the 
lateral portions of the upper maxillae begin first anteriorly at about 



Gray's Anatomy. 



ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH ib"i 



the eighth week, and progress posteriorly until complete at about the 
eleventh. Malformations tine to non-union, therefore, date from 
this period, and consist of the following typical varieties: 

Fig. s "> 



Fig. 84 





Cleft of hard and soft palate; rudimen- 
tary intermaxillary bone placed in advance 
of lips. (Mason.) 



Cleft cf hard and soft palate. 
Mason.) 



Fig. s6 




>"T^&-* 



Median fissure of the lower lip and chin. (Marshall, after WofleiO 

1. Non-union of lip on one or both sides— simple hare-lip. 
< 2. Non-union of lip and of maxilla and intermaxillary bone on one 
side (hare-lip. Fig. S4). 

3. Non-union of lip and intermaxillary bone on both sides (double 

hare-lip, Fig. 81). 



158 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 

4. Non-union of all horizontal processes in the median line (cleft 
palate, Figs. 84 and 85). 

5. Non-union of halves of soft palate (cleft velum). 

6. Non-union of halves of the uvula (bifid or cleft uvula). 
Combinations of cleft velum and cleft palate or of cleft palate and 

single or double hare-lip may exist. 

Figs. 81, 82, 84, and 88 show the parts in their ununited state. 

The failure of the inferior maxillary processes to unite is rare, 
but is occasionally seen (Fig. 86). The inferior maxillary tubercles 
develop a transitory support to the lower jaw known as Meckel's 
cartilage. The cartilages of the right and left side do not fuse 
together at the future symphysis. (Hertwig.) (See Figs. 82 and 87.) 

Fig. 87 Fig. 88 





M.C. 



Showing Meckel's cartilage (M.C.) in Osteology of hare-lip. (Museum of the 

longitudinal and transverse section. Philadelphia Dental Coellge.) 

It acts as a support to the fetal jaw, undergoes atrophy at about 
the sixth month of gestation, and at birth but few fragments are 
found near the symphysis. At birth ossification has occurred, and 
the bone consists of two halves united by a fibrous symphysis in 
which ossification takes place during the first year. 

The end of the cartilage in the base of the inferior maxillary process 
becomes the future malleus (one of the bones of the middle ear) . The 
portion of the cartilage running from the malleus to the formed bony 
lower jaw becomes transformed into the internal lateral ligament of 
the inferior maxilla. (Hertwig.) 

A case of failure of development of the intermaxillary bones has 
been reported, 1 the space between the cuspid teeth being about 
one-eighth inch. 

1 Jeffery, British Dental Journal. July, 1904. 



DEVELOPMENT OF THE TEETH 



59 



It is to be remembered that these processes are formed by the out- 
growth of the mesoblastic layer of the blastoderm, and are covered by 
epithelial tissue springing from the epiblast. Both are concerned in 
the formation of the teeth. Epithelium is reflected over the face and 
oral cavity. All tissues between these layers of epithelium excepting 
the dental band and enamel organs and the nerves are of mesoblastic 
origin. 

DEVELOPMENT OF THE TEETH. 

At about the sixth week of gestation, while the maxillary processes 
are but ill-defined masses of mesoblastic tissue surrounded on all 
sides by epiblastic tissue (Fig. 89), the "dental band" develops 
as a continuous depression of 

the stratum Malpighii of the FlG - 89 

mucous membrane extending 
from end to end of the fetal 
jaw (Figs. 90, b, and 91, b), 
over which depression is a 
mound of epithelial cells de- 
veloped from it, and called 
the "dental ridge" (maxillary 
rampart of Kolliker and Wal- 
deyer (Fig. 92, mr). 

At ten points on these bands 
in each jaw, at about the 
seventh to the eighth week, 

a further depression of the Porcine embryo: ep, epithelium, infant 

Stratum Malpighii OCCUrS, of a layer or stratum Malpighii; ct, embryonal 

connective tissue with large intercellular 
more Or leSS denmte Saccular interspaces. 1.5 cm. X 250. (Sudduth.) 

form, the sac also containing 

embryonic epithelial cells (Figs. 90, c, and 92, 3). This enlarges by an 
interiorward growth of epithelial cells, while the attachment to the 
mucous membrane remains constricted. At the ninth week the 
mesoblastic tissue beneath has somewhat condensed, evidencing 
the first appearance of the dentinal papilla. At this stage the cord 
(enamel organ) has been likened in appearance to a Florentine flask 
(Fig. 93, 2). The dentinal papilla pushes up the base of the enamel 
organ, which gradually adapts itself over the papilla, assuming 
first the shape of a Phrygian cap (Fig. 94), and finally a saddle shape 
.(Fig. 95). Just before the connection of the enamel organ with the 
epithelium of the mucous membrane is lost (as shown in Fig. 95) ; the 
cord for the corresponding permanent tooth is given off from the side 
of the temporary cord. Fig. 95, cp, shows this after the separation. 




KM) ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 



Fig. 91 



At the sixteenth week the enamel organ has developed so as to 
contain three distinct formative parts concerned in enamel deposition. 

1 . Next to the papilla the cells of the stratum Malpighii develop 
into nucleated columnar cells, collectively defined by an inner and 
an outer limiting membrane; 
the ameloblasts, the office of 
which is to deposit enamel 
(Fig. 97, e, and Fig. 99, c). 

2. Those next interior de- 
velop into large cells nutri- 
tivelv associated with the 



Fig. 90 




Vertical section through band 
from jaw of porcine embryo: ep, 
epithelium; b, band; c, cord; ct, 
connective tissue. 3.5 cm. X 60. 
(Sudduth.) 



Longitudinal transverse section of the 
inferior maxilla of a porcine embryo: b, 
band, solid at anterior portion, but divided 
posteriorly into band and lamina. 3 cm. 
X 40. (Sudduth.) 



ameloblasts and collectively called the stratum intermedium (Fig. 
99, b); also shown in Fig. 97 between b and c). 

3. Those in the central portion of the enamel organ are large cells 
rich in calcific material and polygonal from mutual pressure, and 
called collectively the stellate reticulum. They furnish the first 
nutritive material for the enamel cells (Fig. 94, 1, and Fig. 97, a). 

The dentinal papilla develops a reticulum of bloodvessels, nerves, 
and branched stellate connective-tissue cells lying in a gelatinous 
matrix. Upon the surface of the papilla elongated nucleated con- 
nective-tissue cells called odontoblasts are found, the office of which 
is to deposit dentin (Fig. 99, e; also Fig. 122, Od.). About the enamel 



DEVELOPMENT OE THE TEETH 



161 



organ and dentinal papilla a fibrous sac develops from the mesoblastic 

tissue, incloses them, and is called the follicle wall (Fig. 95, c. ct.), 
and will become the pericementum or cementum organ. The entire 
wall and its inclosures are called the dental follicle (Fig. 95). At the 
sixteenth week the cord of the temporary enamel organ gives off 
from its side a cord which will form the enamel organ of the suc- 
ceeding permanent tooth, and a cord is given off from the mucous 
membrane for the first permanent molar (Fig. 95, cp.). At the seven- 

Fig. 92 




Section of jaw, embryo of pig, showing growth of enamel organ: 1, epithelium; 
2, stratum Malpighii; 3, first stage in growth of enamel organ of temporary tooth; 
4, embryonic connective tissue; 5, developing bone of jaw; mr, maxillary rampart. 
(Andrews.) 



teenth week dentin deposition begins by the extrusion of small 
calcospherites formed within the odontoblasts, composed chemically 
of calcium and magnesium salts combined with albumin, a combina- 
tion known as calcoglobulin. A cement substance is formed within 
the odontoblasts in a manner similar to the formation of inter- 
prismatic substance in the ameloblast (Fig. 101). This is extruded 
and the calcospherite pushed into it. An examination of Fig. 123 
shows this (as black lines). These calcospherites are evidently piled 
11 l 



102 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 

into the cement substance previously deposited against the amelo- 
hlasts, and later against each other, and around protoplasmic pro- 
longations of some of the odontoblasts, which prolongations remain 
in similarly compiled tube-like structures known as tubule walls or 
sheaths of Neuman, while the odontoblasts themselves recede, leaving 
behind them a portion of their substance in the tubules, and known 



Fig. 93 



m 




Section of jaw, embryo of pig, showing growth of enamel organ: 1, epithelium; 
2, second stage in growth of enamel organ; 3, embryonic connective tissue. (Andrews.) 



as the dentinal fibrils. They finally persist upon the surface of the 
pulp (Figs. 99, 100, 110, 122). Fig. 123, a stained specimen of formed 
dentin, shows the arrangement of the compiled calcospherites. It 
is apparently almost analogous to enamel formation. After some 
dentin has been deposited enamel deposition begins (at about the 
fifth month) . The ameloblasts in like manner form within themselves 
calcospherites or enamel globules, also an amorphous substance 



DEVELOPMENT OF THE TEETH 



163 



called interprismatic cement substance, Both are calcoglobulin, and 

yet contain less organic matter, at least finally, than the dentinal 
calcoglobulin. 

The ameloblast first extrudes a drop of interprismatic cement 
substance against the dentin, and into it deposits an enamel globule. 
(Williams.) (Fig. 101, e.) This is repeated, the ameloblasts mean- 
while receding, the result in finished enamel being a rod composed 
of enamel globules united in a row by intervening layers of inter- 



Fig. 94 




Section of jaw, embryo of pig, showing growth of enamel organ and dentin germ: 
1, enamel organ; 2, dentin germ; 3, growth of jaw; 4, tongue. (Andrews.) 



prismatic cement substance. Williams demonstrates plasmic strings 
which unite the various enamel globules to each other — probably 
these give the accurate relation end to end. The scheme of formation 
is shown in Fig. 101, and the orderly arrangement in Fig. 118. The 
hexagonal arrangement shown in transverse section (Fig. 119, B) is 
due to mutual pressure of the globules. Each rod is united laterally 
to its neighbor by interprismatic cement substance, which flows 
there during deposition of each layer of the enamel. The striae of 
the enamel represent periods of incremental activity. That the 



164 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 

enamel rod is not formed by calcification of the ameloblast is proved 
by the fact that the ameloblast lies at an angle to the developing rod. 



Fig. 95 







Vertical transverse section of jaw of porcine embryo, injected: ep, epithelium, 
with (il) infant layer; a, layer of ameloblasts; o, layer of odontoblasts; cp, cord for 
permanent tooth; ot, outer tunic; it, inner tunic; sr, stellate reticulum; wh. ep, 
whorls of epithelium forced from outer tunic and stellate reticulum; d, dentin; dp, 
dentinal pulp; v, bloodvessels of pulp; ct, connective tissue; c. ct, follicular wall; 
p, periosteum; sp, space. 10 cm. X 60. (Sudduth.) 

The function of the stellate reticulum is to furnish calcoglobulin for 
the first enamel deposition. This is probably elaborated in the 



DEVELOPMENT OF TIIF TKKTU 



165 



stratum intermedium and passed on to the ameloblasts, which con- 
struct the calcospherites and interprismatic cement substance. After 
the first deposition of enamel the stellate reticulum disappears and 
the papilla-like structure of the stratum intermedium comes into 
relation with the capillaries of the follicle wall, from which its cells 
derive further nutrition and become the originators of the calco- 
globulin used in enamel deposition (Fig. 101, D, in which b of Fig. 
97 is supposed to have disappeared). After enamel completion the 
ameloblasts and remains of the enamel organ persist as Nasmyth's 
membrane, a structure epithelial in character, ^tttt in. in thickness 

Fig. 96 




Nasmyth's membrane, showing marks of hexagonal ends of enamel prisms. (Section 

by Barrett.) 

(Hopewell-Smith), and quite resistant to acids. Andrews 1 describes 
this as somewhat horn-like and believes it due to a final merging of the 
ameloblasts and cells of the stratum intermedium with an imperfect 
degree of calcification. M. T. Barrett shows that its under surface 
may bear the hexagonal impress of the enamel rods (Fig. 96). As 
the tooth is pushed up the enamel organ is carried with it, but leaves 
behind it epithelial remnants which become included in the follicle 
walls as the epithelial root sheath of Hertwig (Fig. 98). These are 
claimed by Hertwig to be epithelial remains or resting cells in the 
pericementum, which have been described by Black as pericemental 
glands. As shown by Kirk, these structures have been previously 
described by Hertwig as an epithelial root sheath, the remains 



Dental Cosmos, 1912, p. 53. 



L66 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 

or trailings of the enamel organ left as the tooth advances through 
the area previously wholly occupied by the enamel organ. During 
the development of the follicle, bone is formed in islets which appear 

Fig. 97 

- — W UWWM PI -r 



\ 




Section of developing tooth of an embryo calf: a and b, nuclei of reticulum of 
enamel organ, showing spongiose character; c, outer ameloblastic membrane; d, 
inner ameloblastic membrane; e and /, enamel globules faintly showing nuclear net- 
work. X 1000. (Williams.) 



in the mesoblastic structure betw T een the follicle w r all and the peri- 
osteum (Figs. 92 to 95). These gradually coalesce until a bony wall 
is formed which constitutes the greater bulk of the fetal jaw. The 
cavities in the bone are called crypts, are divided by septa, and are 



DEVELOPMENT OF THE TEETH 



167 



nicely shown in Fig. 104, which also shows the relation of three per- 
manent tooth sacs to those of their predecessors. In this figure the 
outer plate of hone is removed, and one is looking at the outside of 
the sac or follicle wall, of which Fig. 102 is a transverse section. 



Fig. 98 




Developing tooth showing Nasmyth's membrane over enamel; also. Hertwig's root 
sheath. (See text.) (Section by Addison.) 



Fig. 102 shows a dental follicle in an advanced stage of enamel and 
dentin development, viz., at birth. Root formation then begins, and 
is carried on by the odontoblasts in the papilla and cementoblasts in 
the follicle wall (Fig. 110). The odontoblasts in the papilla form 
dentin, which protrudes beyond the dentin covered by enamel. 
In this first formed dentin are spaces containing organic matter, and 
collectively known as the granular layer of Tomes (Fig. 124, J). The 
tubules near this are highly branched and anastomotic. Coinci- 
dently with dentin formation the osteoblasts in the follicle wall also 
develop within themselves calcospherites and probably cement sub- 
stance, which together they deposit as cementum against the dentin 
as a modified bone (subperiosteal deposition) and recede, leaving 
some osteoblasts in lacunae (Figs. 105 and 124, K). The finished 
_ cementum shows strata representing periods of incremental activity 
(Fig. 124). It will be noted that the general mode of calcospherite 
and interspherite cement substance formation and deposition is 
practically the same in the ameloblasts, odontoblasts, and osteoblasts; 



168 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 

not as to finished product, but in principle. The follicle wall is 
caught between the developing cementum and bone, and persists as 
a pericementum, the fibers of which attach them to each other (Figs. 
102, C, and 110, PER). Fig. 103 shows the various stages of root 
formation, the bifurcation of roots being effected by an upward pres- 
sure by the follicle wall against the pulp, in the same manner as the 



Fig. 




Section of developing tooth of an embryo calf: a, stellate reticulum of enamel 
organ; b, stratum intermedium; c, ameloblasts; d, dentin; e, odontoblasts; /, blood- 
vessels — corpuscles in situ. X 275. (Williams.) 



enamel organ is indented by the papilla. The lower first permanent 
molar in Fig. 115 and the third figure in Fig. 103 show plainly, by the 
aid of a little imagination, how this is accomplished. The dia- 
gram (Fig. 107) gives the ages at which root calcification is complete 
in the temporary set. The end of the root is composed entirely of 
cementum and is therefore finished by the follicle wall (pericemen- 
tum). 



DEVELOPMENT OF THE TEETH 
Fig. LOO 



L69 



n- \ w\ \ 







* 



iVi ; ! ' v 



Section of growing tooth of calf at birth, showing fibrils, fibril cells, and odontoblasts 
also the layer of calcoglobulin and the forming dentin. (Andrews.) 

Fig. 101 




Mode of enamel deposition: A, formed enamel; B, ameloblasts; C, secreting 
.papillae of stratum intermedium; D, bloodvessels in external fibrous coat and to 
secreting papillae; E, enamel globules with connecting plasmic strings; F, nuclei 
of ameloblasts; G, blood supply of odontoblastic layer; H, odontoblasts; I, un- 
formed dentin; J, formed dentin. The interprismatic cement substance is shown as 
smaller bodies within the ameloblasts. Semidiagrammatic. (Williams.) 



170 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 

The Permanent Teeth. — These are nearly all formed from cords 
given off at the sixteenth week from the sides of the cord of the corre- 
sponding temporary teeth 
Fig. 102 as far back as the bicus- 

pids, which are given off 
from the cords of the 
first and second tempo- 
rary molars (Fig. 95) ; the 
sacs are formed and lie 
lingual to and above the 
sacs of the temporary 
teeth (Fig. 113 and 114). 
At the fifteenth week of 
fetal life the cords of the 
first permanent molars 
are given off from the 
mucous membrane, at 
the third month after 
birth the cord for the 
second molar is given off 
from that of the first 
molar, and at three years 
after birth the cord of the 
third molar arises from 
that of the second molar. After eruption and root completion in the 
temporary teeth and some development of the crowns of the perma- 

Fig. 103 




Developing tooth at birth : A, developing bone; 
B, tissue reflected from follicular wall and forming 
alveolar periosteum; C, follicular wall; D, vessels 
and nerves; E, epithelium of gum. 



WM-m 



Pulp cavities of the superior first bicuspid, from the seventh to the twelfth year. 

(Broomell. 1 ) 



nent teeth the relation of the crypts of the permanent teeth to the 
temporary teeth is as shown in Figs. 112 to 115. 

1 Anatomy and Histology of the Mouth and Teeth. 



DEVELOPMENT OF THE TEETH 



171 



The roots of the permanent teeth are developed during the period 
of the descent of their crowns into the alveoli of the temporary teeth, 



Fig. 104 




1, tooth sacs of deciduous teeth turned out of crypts; 2, lingual surface of mandible. 
The interior of the crypts and septa shown. (Broomell.) 

which occurs coincidently with the resorption of the temporary roots, 
which permits the descent. After the shedding of the deciduous teeth 

Fig. 105 




Transverse section through fused roots of molar tooth, showing interdentinal 
cementum: 1, interdentinal cementum. X 30. (Broomell.) 



and the eruption of the permanent ones the roots are completed after 
variable periods, graphically shown in Fig. 116. Coincidently with 



172 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 

this the jaws enlarge in all directions by resorption and new depo- 
sition of hone. Both the development of the crowns and roots are 
similar to those occurring in the temporary teeth. 

Fig. 10G 




Persistence of Nasmyth's membrane in occlusal fissure. (M. F. Barrett.) 

The Histology of the Teeth. — Some of the histology of the teeth 
has been given with the description of the development of the teeth, 
and extended explanation is unnecessary in a work devoted to dental 
pathology. Some of the structures, however, require some notice as 
a basis for pathological variations, and will be specially described. 



Fig. 107 



22 months after birth 
18 months after birth 

12 months after birth 



6 months after birth 

40th week (birth) 
30th week embryo 
18th week embryo 
17th week embryo ■ 



1LJTR 







Calcification of the deciduous teeth. (Peirce.) 



The Enamel. — The rods radiate as shown in Fig. 117, but in the 
fissures Nasmyth's membrane persists and rarely completes a perfect 



DEVELOPMENT OF THE TEETH 



173 



groove, so that a convenient location for food and microorganisms 
remains, and dental caries is most common at this point. The 
rods are wavy in outline, though sometimes twisted or gnarled. 



Fig. 108 




Injected tooth, showing connection between dentinal tubules and lacuna? of 
cementum. (Von Beust.) 



Fig. 109 




Injected tooth, showing connection between dentinal tubules and enamel tubes. 

(Von Beust.) 



They are hexagonal in cross-section (Fig. 119). The enamel is thin at 
the cervix, and is usually overlapped by the cementum, but may 



174 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 



overlap it, or lie edge to edge with it (Choquet). The striae of 
Retzius are pigmented bands, or colored increment. The stripes 
of Schreger are cloud-like markings, shown by Caush to be due to 
the presence of tubes in the enamel and containing organic matter. 
Caush and, later, others have shown that the enamel contains 
tubes into which the dentinal fibrils penetrate (see Figs. 179, 182, 
and 184). The outer surface also may contain openings indicative 
of present or past organic contents. Each rod is composed of 



Fig. 110 



Fig. Ill 





Condition of third molar 
at thirteen years of age. 
(Skiagraphed by Custer.) 



Fig. 112 



Diagram illustrating root development and 
condition of an incomplete root: E, enamel; 
D, dentin; P, pulp containing odontoblasts, 
OB; AP, alveolar process; B, bone; C, cemen- 
tum; P', periosteum of bone continuous with 
the pericementum; PER, pericementum con- 
taining cementoblasts, CB; A, V, N, arteries, 
veins, and nerves. 




Showing the relation of per- 
manent tooth follicle to the 
root of the temporary tooth. 



enamel globules united end to end by interprismatic cement sub- 
stance, which also unites adjoining rods longitudinally (Fig. 118). 
Von Beust 1 has shown by injecting pulp canals with a strong solution 
of fuchsin, also by an arrangement merely dipping the root apex in the 
above solution, that force or even capillarity will carry the staining 
fluid through the dentin into enamel and cementum (see Figs. 

Dental Cosmos, June, 1912, p. 660 and 662. 



Fig. 113 




Tooth follicles for deciduous and permanent teeth, three months after birth: 1, 2, 
tooth sacs of deciduous teeth; 3, periosteum of hard palate; 4, tooth sacs of permanent 
teeth. (Broomell.) 

Fig. 114 




Deciduous molars with tooth sacs for permanent bicuspids attached to the gingival 

tissue. (Broomell.) 



Fig. 115 




View of the upper jaw of a child, aged about six and one-half years. The anterior 
teeth are slightly separated by the partially developed permanent teeth, lying behind 
or posterior to them, pushing forward to occupy a more anterior position. The equal 
height which the crowns of the deciduous teeth originally occupied is also being dis- 
turbed by the advancing permanent teeth. (Peirce.) 



170 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 



E 


03 


03 


03 


B 


03 


a a^ 


6 

b 

03 


- 


crt 


crt 


Kl 


crt 


crt 


03 rf J) 


o 


o 


(!) 


(1) 


<D 


0) 


D O ^ 


>. 


>a 


>> 


>5 


>> 


>> 


>> >> £ 


o 


GO 


co 


^ 


(M 


O 


Oi 00 »o 


7\ 


<-* 


f-i 


"— ' 


•H 


>— ' 


(N 



107 and 108), and shows conclusively the presence in enamel of canals 
communicating with the dentinal tubules and at least permeable by 
fluids; also that the dentin and cementum communicate by canals. 

The Dentin.— The dentin 
is composed of tubules and 
their contents and intertub- 
ular substance. Each tubule 
contains a prolongation of an 
odontoblast, also called a 
"fiber of Tomes/' or denti- 
nal fibril. The wall, differing 
from intertubular dentin, is 
called the sheath of Neuman 
(Fig. 121). 

The tubules are wavy in 
direction, but radiate in the 
crown and lie at right angles 
to the pulp in the root den- 
tin. At the periphery the 
tubules branch and anasto- 
mose freely, and some may 
penetrate the enamel. There 
are also fine anastomatic 
connections at other points 
(Fig. 121). Both the tubules 
and intertubular substance 
seem to be composed of cal- 
cospherites and cement sub- 
stance (Fig. 123). 

The tubules are curved in 
outline and sometimes show 
a series of short, sharp 
curves on a general curved 
level at the points at which 
a new period of increment 
has occurred. They are the 
stripes of Schreger in dentin 
or "incremental lines" of 
Salter (Fig. 190). 

The Pulp. — This consists 
of a gelatinous matrix 
in which are imbedded 
branched connective-tissue 






03 " 


02 

S-H 


03 


03 


03 


to 


02 


t 


CO 




3 


~ 


a 


a 


c3 


03 


C3 


c-> 


Kl 


Cfl 


- 


r: 


CD 


<y 


<x> 


CD 


C<) 


CU 


<d 












>> 


>> 


>, 


>> 


>> 


>> 


>-. 


>> 


>> 


>> 


>> 


X! 


IN 


o 


OJ 


00 


t^ 


o 


10 


^ 


CO 


(N 


^H 


+3 

< 


r - 


1-1 





















Fig. 117 




Diagram of enamel-rod directions and tubule curves. From a photograph of a bucco- 
lingual section of a superior bicuspid. (Noyes.) 



Fig. 118 




Section of enamel of human tooth. Photographed with Zeiss apochromatic lens 
and Powel and Leland apochromatic condenser. The optical parts accurately centred 
and the focus "critical." The enamel rods are seen to be resolved into distinct sec- 
tions (enamel globules), the cement substance often passing entirely between the 
sections. X 400. (Williams.) 
12 ' 



178 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 

cells. The odontoblasts lie upon the surface next to the dentin, 
with their fibrils extending into the tubules up to the enamel, and, 
as shown by Caush, often into it, forming organic matter in enamel, 
and in some cases accounting for a sensitivity which is, however, 
rare. 

Fig. 119 
A 





Enamel prisms: A, fragments and single fibers of thi ecamel isolated by the action 
of hydrochloric acid; B, surface of a small fragment of enamel, showing the hexagonal 
ends of the fibers. X 350. 

Fig. 120 



Enamel showing both striation and stratification. X 80 (about). (Noyes.) 



One or more arteries enter the apical foramen or by several fora- 
mina, and several veins may emerge. The arteries subdivide in the 



Fig. 121 



D.C.- 



N.Sch. 














©^ 



Transverse ground section through the dentinal tubules of the first molar of a child, 
aged seven years: V, small connecting tubule. Koch's and Golgi's methods combined. 
X 1200. (Rose.) 

Fig. 122 



(.£>. 



UJ). 




T.I. 



-Od. 



Section of pulp, showing the relations of the odontoblasts to the dentin: Od., 
odontoblasts; T.F., Tomes' fibers — odontoblastic processes; U.D., uncalcified dentin; 
CD., calcified dentin; P.C., pulp cells. X 800. (Rose and Gysi.) 



ISO ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 

central portion of the pulp and form a rich network of capillaries 
beneath the odontoblasts. 

The arteries are not branches entering the foramen directly from 
the bone, but rather branches of arteries in the pericementum. 

The arteries of the pulp soon lose almost entirely their muscular 
coat, and their external coat is reduced to an inconsiderable amount 
of fibrous connective tissue. There is little if any anastomosis of the 
arteries of the pulp, so that collateral circulation is impeded, though 
not necessarily prevented, as pathological cases show. The veins 
remain for an unusual distance without a muscular . coat, and are 
stated by Hopewell-Smith to be non- valvular and non-collapsible. 1 
These histological data have great clinical significance. (See Diseases 
of the Pulp.) 

Fig. 123 




Main mass of dentin of a temporary tooth, stained with chlorid of gold, decalcified 
with acetic acid: F, F, dentinal fibers, partly vacuolated; B, B, basic substance, 
traversed by a reticulum. X 1200. (Hart.) 

The vascularity of the pulp decreases with age. " In young teeth 
there are a number of arterial trunks entering the apical foramen, 
which lessen in number as the passage lessens in size." Finally only 
one may enter. (Black.) 

The passage of arteries and veins through a constricted foramen 
has important consideration in connection with pulp diseases. It 

1 Dental Cosmos, 1907. 



DEVELOPMENT OF THE TEETH 



1S1 



lias been shown by Stein 1 that the arterial supply is through the 
hone rather than hy direct arterial continuity. (See Venous Hyper- 
emia of the Pulp.) 

Mummery 2 recently described the nerves of the pulp as follows: 
The nerves enter by several bundles, and if medullated follow the 
course of the bloodvessels, give off lateral branches, then lose the 
medullary sheath, near the periphery of the pulp, where they break 
up into numerous fine fibers, or axis-cylinders, and combine into 
a plexus beneath the odontoblasts (the plexus of Raschow). 

Fig. 124 







Ground section through the root of a human premolar: D, dentin; K, cement 
corpuscles; 0, osteoblasts; Ep, remains of Hertwig's epithelial root sheath or peri- 
cemental glands of BlaGk; 2 /, interglobular spaces. X 200. (Rose.) 

From this plexus fine fibers pass between and around the odonto- 
blasts, which may be inclosed in a fine network. From these net- 
works fine fibers pass into the tubules and continue to the periphery 
of the dentin and into the anastomotic fibrils. 

« The phenomena of sensitive and hypersensitive dentin shown an 
evident physiological connection. The nerves of the pulp do not 

1 Items of Interest. 2 See Dental Brief, 1912, 

3 The editor has taken the liberty of altering the interpretation. 



182 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 

possess tactile sense; so their pains are not localized, but reflected, 
as a rule. The pulp contains no demonstrable lymphatics, though 
lymph spaces probably exist; their office is probably performed by 
the veins, which in other parts may take up this function. 1 The pulp 
becomes more fibrous and less vascular with age. During health it 
preserves the translucency of the tooth through its relation with the 
fibrillse and under certain circumstances renews its formative activity 
and produces secondary dentin. The forms of the pulps and pulp 
cavities are shown in Figs. 128 to 138. 

Fig. 125 



\-KF 



S.J). 




a g 



N.T.- 



B.V.- 



Section of a tooth pulp: B.V., main bloodvessels of pulp; C, origin of capillaries; 
A 7 . T., main nerve trunk; N. F., subdivisions of nerve into fibrillse; Od., odontoblastic 
layer; S.D., secondary dentin; C.G., masses of calcoglobulin. X 30. (Rose and 
Gysi.) 

The Cementum. — The cementum is a modified bone distributed 
over the dentin of the root. It meets the enamel either edge to 
edge, overlaps it, or is overlapped by it (Choquet). In some cases 
they do not meet at all, and leave the dentin exposed. 2 It contains 
lacunas and canaliculi, but only rarely an Haversian canal. It 

1 Green, Pathology and Morbid Anatomy. 

2 Hopewell-Smith, Dental Cosmos, 1909, p. 1375. 



DEVELOPMENT OF THE TEETH 



183 



contains a fibrillar structure, which represents the remains of Shar- 
per 's fibers (Fig. 126). /• 

The physiological function of the cementum is to afford a means 
of attachment of the teeth to the maxillary bones through the medium 
of the pericemental fibers. In case of death of the pulp, and, there- 
fore, of cessation of nutrition of the dentin, the vital relations of the 

Fig. 126 




Two 



fields of cementum, showing penetrating fibers: Gt., granular layer of Tomes; 
cementum not showing fibers; F., penetrating fibers. X' 54 (about). (Noyes.) 



cementum and alveolar process are thus maintained and the use- 
fulness of the tooth assured. Whether the dentin can ever receive 
nourishment from the cementum after pulp death has never been 
scientifically shown, and the fact that it may contain dead and even 
putrefied material while a healthy cementum may persist, renders it 
extremelv doubtful. 



IS! ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 



The Pericementum. -(Syn., Peridental Membrane). The peri- 
cementum is the highly organized remains of the follicle wall. As 
the alveolar bone and cementum develop on either side of it, it forms 
also the periosteum lining the alveolus. It is, therefore, the means by 
which the teeth are retained in their sockets and a certain degree of 
motion permitted. The pericementum subserves the office of a 
membranous attachment not altogether unlike that found in the 
sutures of the cranial bones. 

Fig. 127 




Portion of the side of a root of a tooth, the gum and alveolodental membrane, and 
the edge of the bone of the alveolus. A band of fibers is seen passing over the surface 
of the alveolus and dividing, some passing upward into the gum, others passing more 
directly across to the cementum. Numerous orifices of vessels cut across trans versely 
are seen between the tooth and the bone. (Black.) 

It is considered by some observers that there are two distinct 
portions to the pericementum, cemental and alveolar. Photo- 
micrographs generally do not demonstrate this, and it is a matter 
of difficulty to imagine the pericemental bands divided into two 
portions. 

It is continuous with the periosteum on the outside of the alveolar 
process, as the sutural membrane is with the pericranial membrane. 

Its outline study divides the pericementum into three portions — ■ 
a gingival, an alveolar, and an apical portion. 1 

1 Noyes, American Text-book of Operative Dentistry. 



DEVELOPMENT OF THE TEETH 



1S5 



Fig. L28 




Transverse section of the peridental membrane in the occlusal third of the alveolar 
portion (from sheep): M, muscle fibers; Per, periosteum; Al, bone of the alveolar 
process; Pd, peridental membrane fibers; P, pulp; D, dentin; Cm, cementum. 
(Noyes. 1 ) , 

1 American Text-book of Operative Dentistry. 



ISC) ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 

It is composed largely of white fibrous tissue with interlaced blood- 
vessels, nerves, and glands. It also contains functional cells, fibro- 
blasts, cementoblasts, osteoblasts, and osteoclasts. 



Fig. 129 



Fig. 130 





Fig. 131 



Fig. 132 





Fig. 133 



Fig. 134 





Fig. 135 



Fig. 136 






Longitudinal and transverse sections of upper teeth, showing shapes of pulp chambers 

and their positions. 



DEVELOPMENT OF THE TEETH 
Fig. 137 



187 




Formalin-gelatin casts of pulp cavities, showing pulp irregularities. (Richards.) 

Fig. 138 




Formalin-gelatin casts of pulp cavities compared with the teeth themselves. 

(Richards.) 



L88 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 

The fibrous tissue is made up of principal fibers and indifferent 
fibers. 1 

The principal fibers are grouped for the most part in bands or 
bundles (Fig-. 128). 

Iu the alveolar portion these bundles run for the most part from 
the cementuru to a higher point on the alveolar process. The attach- 
ment is secured by the penetration of the fibers into either structure. 
This secures to the tooth, support against direct pressure into the 
socket and against rotary motion. 

Fig. 139 




Showing the buccal surfaces of the crowns and roots in position. (Oyer.) 



At the apical portion the bands have a fan-like distribution. In 
the gingival portion the fibers are directed outward and slightly 
toward the edge of the alveolar process for tooth support, or outward 
and downward over the edge of the process to become continuous 

1 Noyes, American Text-book of Operative Dentistry. 



DEVELOPMENT OF THE TEETH 



ISO 



with the periosteal fibers, or outward and upward with the sub- 
mucous gingival tissue, to aid in the support of the gum margin. 
Some of the gingival fibers pass from the cementum of one tooth to 
that of the next (Fig. 127). 




Vertical sort ion of a frozen head, rear view. Shows relations of roots of molars and 
the maxillary sinus, and of the maxillary sinus with the frontal sinus. Wire passes 
from the latter through the infundibulum, the hiatus semilunaris, and the ostium 
maxillare, into the maxillary sinus, establishing a connection. (Cryer.) 



190 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 

The bloodvessels of the pericementum are derived from several 
sources: (1) From vessels entering the membrane through the 
Haversian canals of the alveolar process and bone, and anastomosing 
with branches from the descending arteries; (2) from the vessels of 
the outer periosteum, coming over the edge of the alveolar process. 

It has been shown that the destruction of main arteries as the 
infra-orbital or inferior dental does not cause pulp death, hence the 
collateral blood supply is the most important. 

There are comparatively few capillaries. The vessels lie mostly 
in the outer or alveolar half of the pericementum. 

Fig. 141 







t * 

: 




\ i 

! I 
. - - - 


99H 



Diagram of glands of peridental membrane. (Black.) 



This disposition of the arterial blood supply insures nutrition to 
the peridental membrane in case of loss of the apical tissue, as in 
case of apical abscess, and also insures a collateral blood supply 
to the pulps in case of loss of main arterial trunks, as, for example, 
in operations upon the inferior dental canal, in which case pulps do 
not die. 1 

The arteries thus furnishing blood to the teeth are, for the upper 
jaw: The anterior dental branch of the infra-orbital, to the upper 
anterior teeth; the superior dental branch of the alveolar, to the upper 
bicuspids and molars and the bone about their root ends; the descend- 
ing palatine and its anastomotic connection, the sphenopalatine, 
supplied to the palatine side of the upper alveolar process, etc.; the 
alveolar, supplied to the buccal. side of the upper alveolar process. 

1 John Bethune Stein has experimentally proved this by operation of removal of 
the contents of the inferior dental canal. The pulps did not die, and the teeth developed 
as usual. Items of Interest, May, 1910. 



DEVELOPMENT OF THE TEETH 



191 



In the lower jaw the inferior dental artery and its incisor branch 
supply the apical tissues of the lower teeth from the inferior dental 
canal. Its mylohyoid branch supplies the gums and lingual perios- 
teum of the lower alveolar process, the mental branch supplies the 
lower buccal process anteriorly, while a branch of the facial artery 
anastomoses with the mental anteriorly, and the facial sends branches 
to the coverings of the buccal aspect of the lower jaw posteriorly. 

Fig. 142 




Glands of Black. Epithelial structures: Ec, epithelial cord, apparently showing a 
lumen; Cb, cementoblasts; Cm, cenientum; D, dentin. (Seep. 193) (Noyes.) 



With the exception of those branches derived from the facial artery, 
all the blood comes from the internal maxillary artery. Stein has 
shown that the blood is supplied to the pericementum, which, by 
collateral circulation, supplies the pulp. 

The veins return the blood by similar channels. 

The nerves of the pericementum enter by several trunks in the 
apical tissue, and also enter from the alveolar wall and over the 
alveolar edge. While their distribution is not yet fully described, 
some of them possess the tactile sense, as touch upon the teeth is 



Fig. 143 




Longitudinal section: Ej), epithelium lining the gingival space; Gg, gingival gland 
so-called; D, dentin; N, Nasmyth's membrane; Du, duct-like structure stretching 
away toward the gingivus from the epithelial cord, seen at Ec; Cm, cementum, 
separated from the dentin by decalcification. X 50 (about). (Noyes.) 



DEVELOPMENT OF THE TEETH 193 

fully localized. They are derived from the fifth nerve and the sym- 
pathetic. 

The Pericemental Glands. — Black has described gland-like struc- 
tures lying- in the pericementum, nearer the cementum than the 
alveolar wall. These are distributed over the root in a network, as 
shown in Fig. 141. 

They are convoluted cords of epithelial cells invested with a deli- 
cate basement membrane, and can be traced to the epithelium of the 
gingival space, but not to the surface. 

Traces of a lumen have been seen, which, if established as common, 
would constitute them as tubes. Their function is not definitely 
known, but it is presumptive that they may be secreting glands or 
lymphatics. Some consider these glands as resting epithelial cells 
derived from the enamel organ during the upward movement of the 
tooth, i. e. y the epithelial root sheath of Hertwig (Figs. 124, 141, 
and 142). The entrance of bacteria from the gingival space to deep 
portions of the pericementum, there to develop, may possibly be 
favored by their presence. They are also considered as the tissue 
in which cysts arise. (See p. 165.) 

Glands of Serres. — At the deepest portion of the gingival space 
is found a gland-like body which has been given the above name. 
Its function is not known (Fig. 143). 

The Cellular Elements. — The fibroblasts are spindle-shaped cells 
destined to become mature fibers. They lie among the other fibers. 
The cementoblasts lie along the cementum and are the cementum 
builders (Figs. 72 and 110). Osteoblasts are found engaged in 
bone construction along the alveolar wall. 

Osteoclasts, large multinucleated cells, lie at points along the 
cementum of teeth and alveolar bone. Their office is the removal of 
bony tissue. They remove both the organic and inorganic material, 
and their effects are seen upon the cementum and dentin of the 
roots of teeth undergoing resorption, also upon resorbed alveolar 
process. The" excavations in which they lie at work are called 
Howship's lacunas (Fig. 73). 

Calcospherites are sometimes found within the substance of the 
pericemental membrane, and may have some significance in relation 
to its diseases. 

The pericementum in the young is comparatively large and vas- 
cular, and in the old becomes much attenuated, more fibrous, less 
vascular, and subject to degeneration. 

Union of alveolar bone and cementum but rarely occurs, though a 
mechanical attachment by fibrous pericementum may occur. (See 
Synostosis.) On the other hand, the union of the cementum of one 
tooth with that of another is not uncommon. (See Concrescence.) 
13 



CHAPTER VII. 

DENTITION: ITS PROGRESS, VARIATIONS, AND 
ATTENDANT DISORDERS. 

The process of teething, eruption, or dentition comprises that 
series of vital operations which causes the teeth to leave their crypts 
in the maxillae, to pierce the gum, and to take their places in the 
dental arches. It is a continuation of the process of dental develop- 
ment, and is accompanied and succeeded by root, alveolar, and max- 
illary developments, which are also to be considered in connection 
with it. 

Physiologically, dentition is divided into (1) the first dentition, or 
that of the temporary teeth, and (2) the second dentition, or that of 
the permanent teeth. 

Examination of Fig. 102 will show the state of tooth development 
at a period shortly after birth (a central incisor being under con- 
sideration). The crypt is roofed over at birth by a membranous 
structure. During the period from then to perhaps six months after 
birth, about one-third of the root will have been formed. (See Fig. 
107.) The root end is widely open (incomplete) and the margins are 
thin and sharp. A very vascular tissue occupies the space between 
the root and the bone, and fills the interior of the root. Meanwhile 
the crown cusp will have advanced from the situation shown in Fig. 
102 to a point just beneath the mucous membrane, which is pressed 
up and stretched over the advancing tooth crown, presenting to oral 
view a tumefied condition more or less corresponding to the form of 
the crown. This is nicely shown in Fig. 144, A and B. 

These anatomical data serve for the consideration of the causes 
and process of eruption. 

Causes of Eruption. — It is evident that there are forces which 
can bring about the elevation of a tooth crown from its bed in the 
crypt to its position in the mouth. 

The consideration of these has led to the development of the 
following rational theories, as well as others now obsolete: 

1. That crown elevation is due to the lengthening of the root — 
i. e. y as root tissue is formed by the pulp and follicle wall lying beneath 
and to the side of its edges, the tooth is mechanically pushed up, the 
tissues lying above it are stimulated and absorbed, and as more root 



DENTITION 



195 



Fig. 144 



is formed, a further extrusion occurs. It is to be noted that the root 
end occupies the same level, at all stages of eruption, in the devel- 
oping jaw that was occupied by the cervical edge of the crown 
(Fig. 145). As no two bodies may occupy the same space at the same 
time, the root-forming pulp and follicle wall push the tooth up, to 
gain room for more root formation. The mild continued pressure is 
quite competent to do this. The pressure of the soft tissues against 
the root end is explained by Constant to be derived from the normal 
blood pressure. 1 That such an internal pressure exists is shown by 
the extrusion of ordinarily confined parts when released from the 
accustomed pressure. A simple accident demonstrated this to the 
editor. While excavating with 
a large bur, the softened dentin 
about a decayed pulp cham- 
ber, the cementum was widely 
removed from the pericemental 
tissue beneath, which latter 
fortunately remained un- 
broken. It immediately pro- 
truded into the perforation. 
Constant also cites the extru- 
sion of a tooth in pericemen- 
titis as an evidence of the 
influence of the blood press- 
ure. Another evidence is the 
occasional rapid advance of a 
tooth after lancing of the gum. 

2. The process of tooth development is a vital process, and that of 
eruption has been held also to be. (Tomes.) That cells concerned 
in development seem to have a predestined end or function cannot be 
denied; at the same time, throughout dental development, defined 
resistances to opposing forces seem to play a part in the moulding of 
the soft and hard tissues — e. g., the depression of the enamel organ 
by the papilla. 

3. Peirce 2 holds that the impact of blows upon the jaws causes the 
tooth to rise toward the gum. He explains the eruption of crowns 
without roots upon this theory. 

4. Tomes explains the eruption of teeth, after development of the 
root, upon the theory that the closing in of the alveolar process or 
contraction of the alveolus upon the pericementum (follicle wall) 
causes the lifting up of the tooth. That such a closure occurs about 




Lines of incision in lancing: A, A, over 
the molars; B, B, over the cuspids and in- 
cisors before eruption; C, C, C, over the 
molars and cuspids after partial eruption. 



1 International Dental Journal, June, 1903. 



American System of Dentistry. 



L96 



DENTITION 



the extruding roots of teeth left after the breaking away of the crowns, 
is shown by examination of the sockets of such roots. An abnormally 
shallow alveolus closed by deposition of bone at its apex will be found 
in cases of small apical portions of roots so extruded. 

It is well known that mild hyperemia is produced in pericementi 
which do not receive a normal resistance, which would account for 
both the elevation and bone deposition on the ground of blood 
pressure. (See Arterial Hyperemia.) 

Fig. 145 




Diagram showing the upward movement of the crown during eruption and root 
development. (Constant.) 



The Process of Dentition. — At varying ages, according to the 
state of tooth development, the formed crown of the tooth advances 
and presses upon the follicle wall overlying it; this is irritated, and 
giant cells are developed, which by resorption remove this as well 
as the upper edge of the wall of the crypt. The mucous membrane 
is pushed up and moulded over the crown, thereby causing a tume- 
faction. 

The mucous membrane, at first normal in color, becomes slightly 
hyperemic, and then may change to an ischemic condition and whiten, 
owing to the removal of the blood by the pressure of the underlying 
crown. Resorption from beneath causes a break in the continuity of 
the mucous membrane, and the crown tip erupts into the mouth 
(Fig. 144, C). 

The rate of resorption and crown advance are equalized in perfectly 
normal dentition. (See cause of pathological dentition p. 199.) 

The crown rises from the gum, is directed by the tongue and lip or 
cheek, and, finally, meets its antagonists of the opposite jaw. The 
interlocking of cusps and meeting of occlusal surfaces limit further 
movement of position. 

Meanwhile root development proceeds, and as it occurs the alveolar 



DKXTITIOX 



197 



process is built about the pericementum, which consist of the follicle 

wall drawn up. By this means the roots are firmly implanted. 
The further development of the root proceeds until complete, and so 
remains until normal resorption of the temporary roots occurs, and 
for life in the permanent teeth. 

The state of formation of the roots of temporary teeth at any 
given age may be judged by the table of averages shown by Peirce 
in Fig. 107. Being but averages, allowance for delays must be made. 

Apart from the presence of the temporary teeth, the process of 
eruption is identical in both sets of teeth. 

Periods of Eruption. — As a general rule, the eruption of the 
deciduous teeth may be said to begin about the seventh month after 
birth, and is completed somewhere about the twenty-fifth month. 
This rule, however, varies within wide limits; some children may be 
born with teeth erupted; again, the initiation of the process may not 
occur until the twelfth month, or even later. 

The incisor teeth are usually erupted in pairs, the molars and 
cuspids making their appearance in fours, the first molars in cne 
group, the cuspids in another, and the second molars in a third group. 
The several groups require different lengths of time to complete their 
eruption, the time occupied in the eruption of the first molars being 
longer than that required for the eruption of the other groups. 
Between the appearance of additional groups of the teeth an interval 
elapses, no doubt a physiological provision, for, as will be shown 
later, the process of dentition is usually accompanied by evidences of 
more or less local disturbance, frequently by disturbances through- 
out the intestinal tract, and even reflex disorders of the central 
nervous system occur. It is believed, therefore, that the period 
which elapses between the eruption of the dental groups permits 
the organism to recover from the effects of previous disturbance 
before the new source of irritation appears. 

Table. 1 



Group 1 Lower central in- 
cisors 

Group 2 Upper central and 
lateral incisors 

Group 3 Lower lateral in- 
cisors 

Group 4 First molars 

Group 5 Cuspids 
Group 6 Second molars 



Time of eruption, 

7 months 
Time of eruption. 

9 months 
Time of eruption. 

12 months 
Time of eruption, 

14 months 
Time of eruption, 

18 months 
Time of eruption, 

26 months 



Duration of eruption, 

1 to 10 days 
Duration of eruption. 

4 to 6 weeks 



Duration of eruption. 

1 to 2 months 
Duration of eruption, 

2 to 3 months 
Duration of eruption. 

3 to 5 months 



Interval. 2 to 3 month? 
Interval, 2 months. 



Interval, 4 to 5 months. 
Interval, 3 to 5 months. 



Coleman's Dental Surgery (Stelhvagen). 



198 DENTITION 

In the above table it will be noted that the time of eruption of 
the lower lateral incisors is later than that of the eruption of the upper 
lateral incisors. The reverse course is frequently observed; indeed, 
it has usually been accepted as the rule of precedence in the United 
States. All tables, as to periods of eruption, give but the approxi- 
mate times; while variations are extremely common. The ages 
given in this table are those at about which the several teeth may 
be expected to make their appearance. Stellwagen (the American 
editor of Coleman), in commenting upon this table, states that the 
periods of eruption in this country are from one-seventh or more, 
earlier than the dates given. He suggests that the difference in 
food habit may account for the differences in time. 

Accompanying the development and eruption of the teeth, occur 
developmental changes in all of the glandular appendages of the 
alimentary canal ; probably the alterations in their structure, and no 
doubt in their physiological chemistry, are accompanied by dental 
provision for the mechanical subdivision of foods of postinfantile 
character. 

Symptoms of Eruption. — Slight local disturbances are so com- 
mon in even so-called normal first dentition as to be accepted as 
physiological. The resorption of soft tissue around the tip of the 
crown of the tooth implies a condition of mild non-septic inflamma- 
tion at that point. In more marked cases there is evidence of some 
irritation cognizable to the infant; the gum is of a somewhat deeper 
color and its temperature is elevated. Relief is afforded by pressure, 
which temporarily reduces the hyperemia, and the child is pleased 
to have its gums rubbed, to bite upon its own or the nurse's fingers, 
upon rings or other objects. Still more marked is the soothing effect 
of biting upon cold substances, such as ice, which, in addition to 
mechanically lessening the blood supply, causes contraction of the 
dilated vessels. 

Slight reflex disturbances are evidenced by the stimulation of the 
salivary glands, which produces an increased flow of saliva. 

Reflex disturbances of more severe character occur in pathological 
dentition, to be considered later. 



PATHOLOGICAL FIRST DENTITION. 

The local disturbances may be exaggerated beyond that degree 
accepted as physiological, and may be accompanied by nervous, 
alimentary, pulmonary, or cutaneous disturbances. This is patho- 
logical dentition, and may be of several grades of severity. 



PATHOLOGICAL FIRST DENTITION 199 

| Causes and Pathology. — The primary cause of pathological dentition 
may be stated as an inequality in the rate of gum resorption and 
crown advance. The advancing crown pressing upon the gum tissue 
causes irritation; the hyperemia or mild aseptic inflammation result- 
ing, instead of remaining at a point favoring the development of 
giant cells and resorption, passes the physiological point and causes 
a disturbance of function. Inflammation, simple or even infective, 
may occur in the area. ~~7 

Swelling of the gum occurs, winch, being distributed in all direc- 
tions, presses upon the crown, depressing it upon the pulp beneath 
the sharp root margins; at the same time the blood pressure of the 
pulp tends to press the tooth upward. The simple lack of resorption 
of the gum would be almost equally effective in preventing eruption. 

The sharp edges of the root must irritate the sensitive and delicate 
pulp tissue, which becomes inflamed and swollen, and still more 
strongly urges the tooth upward. Two sources of disturbance now 
are possible: (1) the irritated gum tissue and (2) the irritated pulp. 
The latter is the more likely to cause reflex disturbances. Through 
the intimate sympathetic relations of the fifth cranial nerve, supplied 
to the pulp, with the seventh, ninth, and tenth cranial nerves in and 
about the floor of the fourth ventricle of the brain, salivary, muscular, 
nervous, alimentary, and pulmonary disturbances become possible. 

Though the pulp is more likely to produce the reflex disturbance, 
a gum inflammation, if intense, is often capable of producing even 
prostrating symptoms. Any systemic disturbance — e. g., measles, 
general debility, or lesser disturbance, etc. — which lowers the gen- 
eral nutritive function also in the parts associated with the teeth, 
may favor the production of local pathological phenomena. Again, 
systemic disturbance readily produces a hyperesthesia of the nervous 
system, favoring the production of nervous phenomena. 

Pathological dentition may occur in the absence of an evident 
hyperemic gum tissue. The tissue may be white, showing ischemia 
from pressure, a binding down of the root end upon the pulp being 
proved by the subsidence of symptoms after lancing, and sometimes 
by the rapid, partial eruption of the tooth immediately after lancing. 

Again, pathological phenomena have been noted where no super- 
ficial local disturbance was evident. In these cases the deeper tissues 
may exert a restraining influence upon the crown, but the swelling 
is just as probable. 

«It is to be understood that the nervous and digestive systems of 
the child are in a developmental condition, and therefore in unstable 
physiological equilibrium, so that any added physiological w r ork, such 
as unusual growth or dentition, may be more than the organism 



200 DENTITION 

ciiii endure without a definite loss of general vital potential. This 
may be further complicated by hereditary defects of tissue, such as 
neurotic, degenerative, or syphilitic taint, or conditions of hygiene or 
feeding tending to lower the health standard. 

Ottofy offers the following report, by the Bureau of Health of 
Manila, of 3250 deaths before twelve months of age: 

Before completing one month 647 

During second and third months 302 

Various causes not dental 959 

Four to twelve months due to convulsions and eclampsia . . . 1342 

Total 3250 

Showing a large number of deaths due to causes in which dentition 
may have been a determining or complicating factor. 

Dr. William P. Spratley, medical superintendent of an institution 
for epileptics, states it as his opinion that pathological first and second 
dentition is a determining cause of epilepsy in children having 
neuropathic taint in that direction. 1 

Symptoms. — The symptoms of pathological dentition are both local 
and general. 

Local Symptoms. — The local symptoms are usually those of inflam- 
mation, red and swollen gum tissues at times assuming a dusky hue. 
The gums may be white, and often glistening, indicating their tense 
stretching over the crowns. In the gum over the erupting tooth 
there may exist a vesicular enlargement containing fluid. 2 Evidence 
of local irritability is given by the fact that the child resists the 
touching of the gums, seizes the breast or bottle nipple, and imme- 
diately releases it. 

The readiness with which the child will take cold substances, ice 
or iced water, is notable and self -explainable. Alternate, excessive 
flow of saliva and oral dryness are present. 

In the more marked cases of local disturbance, evidences of bacterial 
infection of the mucous membrane of the mouth may make their 
appearance, such as ulcerative stomatitis. While, as a rule, the 
breaking down and ulceration of the tissue are confined to the parts 
overlying the erupting teeth, a general stomatitis or widely scattered 
patches of ulceration may make their appearance. The localized 
condition has been called odontitis infantum. 

General Symptoms.— The general symptoms may be differ- 
entiated into mild and severe. 

The mild symptoms are such as are attendant upon severe and 
painful inflammations about the face at almost any age; thus anorexia, 

1 Dental Cosmos, 1905. 2 Tomes, System of Dental Surgery. 



PATHOLOGICAL FIRST DENTITION 201 

fretfulness, anger, restlessness, sleeplessness, thirst, mild fever, and 
evident desire for the upright position occur. The pain is at times 

paroxysmal, but may become continuous. 

These symptoms subside upon the eruption of the tooth or lancing, 
though erupting cuspids, bound by a ring of tense gum tissue or by 
adjoining teeth, may continue the irritation even when apparently 
erupted (Fig. 144, C). Again, the cuspids may be caught between 
the lateral and first molar. The more severe general symptoms are 
such as are brought about by reflex neuroses. 

The roots of the fifth cranial nerves supplied to the teeth are in 
intimate relation with the roots of the seventh, ninth, and tenth 
cranial nerves in the floor of the fourth ventricle, as well as with 
other cranial nerves. It may be argued upon a priori grounds that 
irritation of the peripheral ends of the fifth in the pulp tissue may 
therefore readily produce neurotic results in the brain, salivary 
glands, skin, lungs, or larynx, intestinal canal, or muscles of the face 
or extremities. 

Taking the intestinal canal as the most complicated example, we 
find the following data: The stomach and intestines are under the 
influence of the pneumogastric nerve, which sends to its muscular 
coats both stimulant and inhibitory fibers. Likewise it sends vaso- 
motor fibers to the intestines, division of which leads to inhibition 
of the muscular fibers of the vessels and leads to vasodilatation 
and a great increase of very watery succus entericus. 1 ) 

Intestinal Disturbances. — That intestinal disturbances may arise 
independently of teething is self-evident. They are most liable 
to so occur during the very period during which teething may be 
supposed to act as a primary cause of intestinal troubles; hence 
differentiation becomes important. 

That the conditions may be associated is also evident. As a rule, 
intestinal disturbances arise from improper feeding, the food acting 
as an indigestible irritant to the stomach and intestines. Even an 
excessive quantity of good breast or bottle milk may, if not regurgi- 
tated, act as an intestinal irritant. The milk of an excited, exhausted, 
or debauched nurse may also act deleteriously. Fermentation due to 
bacteria ensues, and diarrhea and colic are a natural result. 

Musser 2 attributes these cases to development of the Bacillus coli 
communis and Bacterium lactis aeriformis existing harmlessly in the 
normal intestine, but developing under the abnormal conditions. 
« This occurring in warm weather, when the child suffers from 
intense heat has a very debilitating if not fatal result. 

1 Halliburton, Kirke's Physiology, 1896, p. 684. 2 Medical Diagnosis. 



202 DENTITION 

The condition may be viewed as an infective diarrhea following 
a vasomotor disturbance of the intestinal walls, set up by reflexes 
primarily caused by the indigestible food. The vital resistance is 
lowered by the disturbed alimentation and the pain. 

A similar train of circumstances may be caused by teething. 
Peripheral irritation of terminals of the fifth nerve in the pulp may, 
through the tenth nerve, cause a reflex vasomotor dilatation in the 
walls of the intestines — i. e., hyperemia, a condition which favors 
bacterial invasion. Intestinal digestion is disordered, the vital 
resistance lowered, and an infection ordinarily resisted occurs. 

Diarrhea may follow. In either case alimentation is interfered 
with and the general nutrition suffers. The child is debilitated by 
lack of nutrition; moreover, toxic substances are generated in the 
intestine, which cause a toxemia, to which many of the general 
symptoms may be attributed, such as fever, meningitis, stupor, 
coma, and death. The general debility also further interferes with 
the process of dentition. 

Diagnosis. — A diarrhea due to improper feeding would not be 
preceded by symptoms of pathological dentition; would have a 
history of improper feeding, and possibly of unhygienic conditions, 
such as unsterilized milk or milk bottles, filthy surroundings, etc. 
There is a catarrhal diarrhea accompanied by vomiting and constant 
acid, watery stools. The stools may have a chopped-spinach char- 
acter. There is colic due to collections of gas. 

Such an infective diarrhea may readily follow the reflex and 
debilitating effects of pathological dentition, as shown 
above. 

White 1 has noted that a choleraic diarrhea may accompany and be 
a sign of pathological dentition. Barrett 2 states that a diarrhea due 
to dentition will probably be followed by constipation. 

A symptomatic diarrhea will, as a rule, be accompanied by signs 
of pathological dentition at points in the jaws, at which teeth should 
be in process of eruption. 

Nervous Disturbances. — Disorders referable to the central 
nervous system are the most alarming, and are those indicating the 
higher grades of severity of irritation. 

The milder forms of these are faint muscular twitchings and 
evidences of slight cerebral disturbance. 

Either of these may be the result of poisons absorbed from the 
alimentary canal during the course of intestinal fermentation, but as 
cases of even convulsions have occurred without other cause than 

1 American System of Dentistry. 2 Oral Pathology and Practice. 



PATHOLOGICAL FIRST DENTITION 203 

teething apparent, and been relieved by lancing alone, the possibility 
of direct connection between teething and central nervous disturbance 
must be admitted. 

A distressing symptom, not easy to elicit on account of the age of 
the patient, is headache. The child is sleepless, and cries without 
apparent cause; it becomes quiet, partially from exhaustion, and 
after a period again commences sobbing. The indication of central 
disturbance may at times be noted in the contracted pupils of the 
eyes and in throbbing arteries. The usual treatment, the adminis- 
tration of chloral hydrate and potassium bromide, with cold appli- 
cations to the head, furnishes relief which is frequently not complete 
without attention to the dental organs. 

In the more severe and dangerous cases, the evidences of disorder 
of the central nervous system become unmistakable. These appear 
as clonic convulsions or symptomatic eclampsia. While it is probable 
in many cases that reflex irritation from the process of dentition in 
itself is but a secondary cause of convulsions, yet evidence is sufficient 
to warrant its being regarded as a determining factor. In very many 
cases teething convulsions appear to indicate a neurotic family taint, 
and eclampsia may attend many disorders in children of this type, 
notably the mechanical and chemical irritation induced by the 
presence of large masses of indigestible food in the intestines. 

So-called teething convulsions occur usually at a time when several 
teeth are in process of eruption. The onset of the convulsion is 
rarely, although apparently often, sudden. If the child be closely 
observed, it is noted that a period of cerebral disturbance — fretful 
crying, evidences of headache, sleeplessness, etc. — is followed by a 
period of dulness and somnolence, or the child may lie with eyes 
half open. Twitching of one or more groups of muscles may be 
observed; the orbicularis oris and other muscles of the lips, and the 
muscles of the eye, notably the superior and internal recti, may 
contract spasmodically. A common muscular spasm ushering in con- 
vulsions, is that of the abductor muscles of the thumb; the thumbs 
are drawn toward the palms of the hands. The abductor muscles of 
the feet contracting, the feet are drawn inward. This period may 
be ushered in by a sharp cry, the eyes roll upward with the lids 
half open, and consciousness is lost. The symptoms may disappear, 
the child awakening dazed and fretful; or it may sink into sleep. 
Unless the source of irritation be removed, or active therapeutic 
measures be instituted, the eclampsia may return and in severe 
cases be the precursor of death. 

Infantile paralysis of a group of muscles, or even a single muscle, 
has been recorded, lasting from a few days to months, appearing with 



204 DENTITION 

dentition and disappearing after it. In some eases it persists for 
life. 1 Strabismus, if produced, may also persist. 

Skin Disorders.— It is so common as to be almost termed the rule, 
to find that when there are intestinal symptoms there are eruptions 
observable on the skin. The mildest form of these is an herpetic 
eruption about the mouth; in other cases papular and vesicular 
eruptions are observed upon the skin of the body and limbs. 

Occurring within the mouth, infection may be added and ulcerative 
stomatitis may occur upon the gums, tongue, lips, or inside of the 
cheek. 

Pulmonary Symptoms. — Pulmonary irritation may be expressed in 
laryngeal cough attending the eruption of teeth, and disappearing 
thereafter. 

Treatment of Pathological First Dentition. — This may be divided into 
prophylactic and remedial. The prophylactic measures include care 
as to pasteurization of milk or modified milk diet, sterilization of 
bottles, bottle nipples and rings, the prevention of the introduction of 
unclean fingers into the mouth of the child, and the antiseptic care 
of its mouth by frequent washings with a saturated solution of boric 
acid in water. This last may be applied to the mouth on a soft, linen 
rag wrapped on the forefinger. These measures, together with the 
proper feeding, ventilation, and care as to clothing, which should 
give comfort and not be in any way irritating, tend to prevent intes- 
tinal fermentation and to reduce the general irritability of the infant. 

Remedial Measures. — To reduce local hyperemia of the gum 
above an erupting tooth, a common domestic measure is valuable, viz., 
a small block of ice is placed in a corner of a clean napkin, and con- 
fined in place by a thread; the infant places it in its mouth at pleasure 
if old enough, or the nurse permits the child to bite upon it. The 
mechanical effect of biting upon a hard substance has added to it a 
degree of cold which lessens the local vascular engorgement. 

Any severe local irritation about erupting teeth should be relieved 
by thorough lancing of the gum. It is irrational that the child should 
be permitted to suffer from local irritation wdiich may develop into 
more serious complications. 

This operation is performed by dividing the gum lineally over the 
incisors and cuspids before eruption, crucially over the cuspids after 
eruption of the cusps only, crucially over the upper first molar, and 
with an X-incisor over the upper second and lower first and second 
molars (Fig. 144). 

For severe cases Flagg advised the removal of a block of gum 

1 White, American System of Dentistry. 



PATHOLOGICAL FIRST DENTITION 205 

from over a molar. A cut is made parallel with the lingual side of 
the crown, a second parallel with the buccal side, a third parallel 
with the mesial side. A tenaculum is thrust into the block of gum, 
which is drawn tense, and then divided at the distal portion, prefer- 
ably with a pair of curved gum scissors. Lacking these latter, the 
bistoury may be used. 

The cut over the upper incisors should, if possible, be made a 
little to the outside of the cutting edge, that for the lower to the 
inside, in order that their crowns may take a proper direction toward 
occlusion. 

The instrument to be used is a sharp-pointed bistoury, as it 
penetrates well and permits a free draw cut. It is to be wrapped 
with tape or a strip of linen cloth until only one-quarter of an inch of 
the point is exposed. This precaution prevents accidental wounds. 
The child must be securely held by an assistant, the least sympathetic 
available. 

Flagg's method was to place the child upon its back across the 
lap of the assistant, who, in one position, places his left hand over the 
child's eyes, securing the head; his right hand secures the hands upon 
the abdomen, w T hile the legs are held against his body by the right 
arm. The position may be exactly reversed. The feet should be 
placed toward the light for the upper jaw, the reverse for the lower 
jaw. In another position the child sits upon one thigh of the assist- 
ant, the back of the head resting upon the chest, and the hand of that 
side (usually the right) pressed upon the child's forehead to hold the 
head firmly. The other hand and forearm hold the child's hands 
and legs firmly. 

The operator encloses the gum about the part to be cut with the 
thumb and forefinger of the left hand, so that the bistoury cannot 
slip and cut lip, cheek, or tongue. Incision over the erupting tooth 
should be made until the knife-blade is felt to touch the enamel 
surface. The operation of scarifying the gums, making merely a few 
scratches to relieve engorged vessels, is but temporizing with the 
condition; the cut should be of sufficient extent to entirely remove 
tension from above the tooth. The little finger of the right hand may 
rest upon the chin of the child as an additional guard. 

If the child bite, a cork with a string attached for safety may be 
used as a prop. 

More or less bleeeding follows upon the operation, and, as a rule, 
ceases spontaneously. A short period of bleeding is desirable, so that 
vascular engorgement may be reduced. Suckling by the breast or 
bottle usually serves to check the bleeding; the tissues about the cut 
surfaces are compressed by tongue and lips during suckling, and 



206 DENTITION 

bleeding ceases. In the event of the bleeding continuing, the mouth 
should be carefully examined, and a piece of ice in a napkin may be 
given to the child to suck. The child may swallow the blood and later 
regurgitate it. Obstinate bleeding may require the use of styptics, 
but these should be of a character to cause only coagulation of the 
blood, not the destruction of tissue. A little powdered tannin laid 
upon the cut acts promptly, as does also a small amount of powdered 
alum. In some cases the internal treatment may be necessary. 
(See Hemophilia.) 

Death has occurred from hemorrhage due to lancing, in cases of 
presumably hemorrhagic diathesis; so that inquiry as to family 
history would be a wise precaution. Obtaining such a history, the 
gravity of the symptoms alone warrant the operation. In the absence 
of such a history the operation is to be held as trivial. If it occurs, it 
should be treated as indicated. (See Hemophilia.) 

The operation of lancing is warranted, even when the gum may 
be likely to heal over the tooth by formation of cicatricial tissue, 
provided symptoms demand it* It is contra-indicated in diphtheria 
and erysipelas, owing to the danger of infection. 

Shock has occurred in long-continued debilitated cases, and if 
feared, a trifle of brandy in water may be given previous to the 
operation. 

It is within the knowledge of the writer, that a physician has refused 
to lance the gums in a case diagnosticated as cerebral meningitis, 
even when death was prognosticated and though the child was at 
an age rendering pathological dentition possible, and in spite of a 
history of pathological dentition in a previous child at the same age. 
J. Lewis Smith 1 concedes the similarity of occasional symptoms of 
pathological dentition and cerebral meningitis, so that the above 
therapy was foolish, to say the least, and especially so in view of the 
probable death, which did occur. In many desperate cases, lancing 
has effected marvelously rapid recoveries, aided by judicious handling 
of the accessory symptoms, even though all hope from ordinary 
therapy had been abandoned. 

Treatment of Stomatitis. — Should general stomatitis, with or 
without stomatitis ulcerosa, make its appearance, the mouth is to be 
promptly and freely sprayed with a 3 per cent, solution of hydrogen 
dioxid, followed by a spray of potassic chlorate (gr. xx to § j), which 
usually affords prompt relief. Should the spots of ulceration not 
disappear promptly, the mouth and tissues about the ulcer are to 
be guarded by soft linen napkins; each ulcer is dried and touched 

1 Diseases of Children. 



PATHOLOGICAL FIRST DENTITION 207 

with carbolic acid, full strength. The spraying is to be repeated 
at intervals of three hours during the waking period. 

Treatment of Skin Eruptions. — The eruptions which appear 
upon the skin during dentition may be a source of annoyance to 
the child by causing itching. As a rule, measures directed toward 
a regulation of the intestinal functions cause a disappearance of the 
skin affections. If the eruption be widespread and cause much 
itching, a wash of phenol-sodique, diluted to one-third with water, 
usually affords relief. If the surfaces be then dried and talc powder 
dusted over them the condition is much alleviated. About the mouth 
and over excoriated surfaces a zinc oxid ointment is useful. 

Treatment of Intestinal Symptoms. — The fermentative material 
in the bowel, together with the great mass of bacteria present, should 
be removed by the use of a cathartic. It is indicated in both con- 
stipation and diarrhea. Castor oil serves well, and is readily taken 
by children. To lessen the irritation of the bowel, laudanum and 
powdered acacia may be added. 

The following formula may safely be used even at six months of 
age: 

R — Tincturse opii gtt.-x 

Olei ricini fgiss 

Pulveris acaciae 3i.i 

Saccharini gr. ij 

Aquae cinnamomi q. s. ad fgiij — M. 

Sig. — Shake the bottle, and give one teaspoonful each two hours if needed. 

For an additional six months of age, ten drops more of laudanum 
may be added to the general formula. In mild cases, olive oil in half- 
teaspoonful doses may be substituted. 

Following catharsis, antacid sedative astringents and intestinal 
antiseptics are indicated: 

R/— Saloli 5j 

Bismuthi subnitratis 3ij 

Misturae cretae ad fghj — M. 

Sig. — One teaspoonful every four hours. (Biddle.) 

1$ — Tincturae opii gtt. xvj 

Bismuthi subnitratis 5ij 

Misturae cretae f3iss 

Syr. simp. fgiss — M. 

Sig. — Shake well, and give in teaspoonful doses every four hours. (Barrett.) 

Jhe virtues of both formula? may be obtained by including the 
laudanum (gtt. xii) with the salol formula. 

Listerine in 10-drop doses, in water, every three hours, serves 
as an intestinal antiseptic. 



208 



DENTITION 



The gums are, of course, to be lanced at the outset, if the diarrhea 
be due to pathological dentition. Following the intestinal antisepsis, 
the general debility and possible intestinal toxemia (see p. 207) are 
to have careful attention, and the child's food is to be properly 
adjusted to its needs. 

J. Lewis Smith claims that upon the following diet, ill-conditioned 
children under his care in the hospital escape summer diarrhea and 
thrive; the diet is therefore here introduced. 

For children not nourished on breast milk of good quality, and 
those over three months, he recommends the following substitutes: 

1 . Heat barley flour in a double boiler, the water in the outer vessel 
to be kept boiling for five to seven days, to burst the starch granules 
(Robinson's prepared barley flour can be bought). 

2. Take of this flour one tablespoonful, add 25 or 30 tablespoon- 
fuls of boiling water, and boil and mix for five minutes. Cool to 
blood heat, add 1 dram of diastase to change the starch to dextrin 
and maltose. Forbes' diastase or Taka-diastase can be bought. Of 
the latter, 1 grain will change 150 grains of starch to sugar. 

Pasteurize milk by heating for twenty minutes to 160° F. Cool 
quickly on ice and let the cream separate. To two and one-half 
ounces of the upper half, add a little peptogenic milk powder (Fair- 
child's), to peptonize it. He mixes the peptonized milk with three 
and one-half ounces of the dextrinized gruel at a meal, and feeds 
the infant nine or ten times, at two-hour intervals. Before feeding, 
administer a few drops of a digestive ferment. 

For use in emergency, he recommends two heaped teaspoonfuls 
of condensed milk to fifteen teaspoonfuls of boiled water, as equiva- 
lent to seventeen teaspoonfuls of ordinary milk. 

He gives the following table of quantities of food required by 
infants; either breast or modified cow's milk to be used. 









Ni 


ruber of 


Total daily 


At each feeding. 






daily 


feedings. 


quantity. 


During the first week . 


1 


ounce 




10 


10 ounces 


At the third week . 


H 


ounces 




10 


15 


At the sixth week . 


2 


" 




8 


16 " 


At the third month 


3 


" 




8 


24 " 


At the fourth month 


4 


" 




7 


28 " 


At the sixth month . 


6 


" 




6 


36 " 


At the tenth to twelfth month 


8 


" 




5 


40 " 



White, following Starr, gives the following schedule of the diet of a 
hand-fed infant from birth upward, 1 which will serve as a suggestive 
and useful guide: 



Diseases of the Digestive Organs in Infancy and Childhood, by Louis Starr, M.D. 



PATHOLOGICAL FIRST DENTITION 209 

Diet During the First Week. 

Cream fohi 

Sugar of milk iir. xv 

Whey fSss, f 3 i-i 

Water fgss, f3ij 

This portion to be given every two hours from 5 a.m. to 11 p.m., and in some instances 
once or twice during the night. 

Diet from the Second to the Fifth Week. 

Milk f5ss 

Cream f3ij 

Sugar of milk gr. xv 

Water 15J 

This portion to be given every two hours from 5 a.m. to 11 p.m. 

Diet from the Fifth Week to the End of the Second Month. 

Milk f5J,f3i.i 

Cream f5ss 

Sugar of milk gr. xxx 

Water fgj, f 3ij 

This portion to be given every two hours. 

Diet During the Third Month. 

Milk . -. fgiiss 

Cream fgss 

Sugar of milk 5.1 

Water f § j 

This portion to be given every two and one-half hours. 

Diet During the Fourth and Fifth Months. 

Milk f 3 iiiss 

Cream fgss 

Sugar of milk 5J 

Water f§j 

This portion to be given every three hours. 

Diet During the Sixth Month. 

Milk fgivss 

Cream fgss 

Sugar of milk 3.1 

Water f 3 J 

This portion to be given four times daily. 

Two other meals — morning and mid-day — may be as follows: 

Milk fgivss 

Cream fgss 

Mellin's Food 3.i 

Hot water fg j 

Dissolve the Mellin's Food in the hot water, and add, with stirring, to the previously 
mixed milk and cream. 

In the seventh month, the Mellin's Food may be increased to two 
teaspoonfuls and given three times daily. 

14 l 



210 DENTITION 

Throughout the eighth and ninth months, five meals a day will be 
sufficient — at 7 and 10.30 a.m., 2, 6, and 10 p.m. 

Milk fgviss 

Cream fgss 

Sugar of milk 3J 

Water . . f5j 

This portion for the first and last meals. 

For the other three meals, 1 tablespoonful of Mellin's Food may be 
added, or 1 teaspoonful of "flour-ball" may be given twice daily, 
instead of the Mellin's Food — say at the second and fourth meals. 

Diet tor the Tenth and Eleventh Months. 

First meal, 7 a.m.: 

Milk fgviiiss 

Cream . . f 5 ss 

Mellin's Food gss 

(Or "flour-ball" or barley jelly 5ij) 

Water f§j 

To be used only when Mellin's Food is employed. 

Second meal, 10.30 a.m. : Eight ounces of warm milk. 

Third meal, 2 p.m.: The yolk of an egg lightly boiled with stale 
bread crumbs. 

Fourth meal, 6 p.m.: Same as first. 

Fifth meal, 10 p.m. : Same as second. 

On alternate days the third meal may consist of 1 teacupful (fgvj) 
of beef tea containing a few stale bread crumbs. 

Beef tea, for an infant, is made in the following way: One-half pound 
of fresh rump steak, free from fat, is cut into small pieces, and put 
with 1 pint of cold water into a covered tin saucepan. This must 
stand by the side of the fire for four hours, then be allowed to simmer 
gently (never boil) for two hours, and, finally, be thoroughly skimmed 
to remove all grease. 

A further variation can be made by occasionally using mutton, 
chicken, or veal broths instead of beef tea. 



DIET FROM THE TWELFTH TO THE EIGHTEENTH MONTH 
(FIVE MEALS A day) 

First meal, 7 a.m. : A slice of stale bread broken and soaked in a 
breakfastcupful (fgviij) of new milk. 

Second meal, 10 a.m.: A teacupful of milk (f§vj) with a soda 
biscuit or thin slice of buttered bread. 

Third meal, 2 p.m. : A teacupful of beef tea (fg vj) with a slice of 
bread, 1 good tablespoonful of rice, and milk pudding. 



PATHOLOGICAL FIRST DENTITION 211 

Fourth meal, 6 p.m.: Same as first. 

Fifth meal, 10 P.M.: One tablespoonful of Mellin's Food with 
1 breakfastcupful of milk. 

To alternate with this: 

First meal, 7 a.m. : The yolk of one egg slightly boiled, with bread 
crumbs; 1 teacupful of new milk. 

Second meal, 10 a.m.: A teacupful of milk with a thin slice of 
buttered bread. 

Third meal, 2 p.m.: A mashed boiled potato, moistened with 4 
tablespoonfuls of beef tea; 2 good tablespoonfuls of junket. 

Fourth meal, 6 p.m.: A breakfastcupful of new milk with a slice 
of bread, broken up and soaked in it. 

Fifth meal, 10 p.m.: Same as second. 

The fifth meal is often unnecessary, and sleep should not be dis- 
turbed for it. At the same time, should the child awake an hour or 
more before the first meal time, he should break his fast upon a cup 
of warm milk, and not be allowed to go hungry until the set breakfast 
hour. 



DIET FROM EIGHTEEN MONTHS TO THE END OF TWO AND ONE- 
HALF YEARS (FOUR MEALS A DAY) 

First meal, 7 a.m.: A breakfastcupful of new milk; the yolk of 
one egg lightly boiled; two thin slices of bread and butter. 

Second meal, 11 a.m.: A teacupful of milk with soda biscuit. 

Third meal, 2 p.m.: A breakfastcupful of beef tea, mutton or 
chicken broth, a thin slice of stale bread, a saucer of rice, and milk 
pudding. 

Fourth meal, 6.30 p.m.: A breakfastcupful of milk with bread 
and butter. 

On alternate days: 

First meal, 7 a.m.: Two tablespoonfuls of thoroughly cooked oat- 
meal or wheaten grits, with sugar and cream; 1 teacupful of new 
milk. 

Second meal, 11 a.m. : A teacupful of milk with a slice of bread and 
butter. 

Third meal, 2 p.m.: One tablespoonful of underdone mutton, 
pounded to a paste ; bread and butter, or a mashed potato moistened 
with good plain dish gravy; a saucer of junket. 

fourth meal, 6.30 p.m.: A breakfastcupful of milk, a slice of soft 
milk toast, or a slice or two of bread and butter. 

The foregoing schedule must, of course, be regarded as an average. 
Many children can bear nothing but milk food up to the age of two 



212 DENTITION 

or even three years, and provided enough be taken, no fear for their 
nutrition need be entertained. The rule to adopt is, if a child be 
thriving on milk, it is never to be forced to take additional food, 
merely because a certain age has been reached. Let the healthy 
appetite be the guide. 

The following is recommended by Starr as a modified milk diet, 
and as a substitute for mother's milk while weaning: 

Pasteurized cream fSss 

Pasteurized milk fgiiss 

Sugar of milk 5ss 

Water, boiled . fSj 

Should this not satisfy the infant, increase the ingredients (except cream) to 6, 8, 
or 12 ounces. 

Hare 1 recommends the following diet list, followed in his hospital 
practice : 

DIET FOR A CHILD AGED TWO YEARS. 

Breakfast, 7.30 a.m.: Milk. The lightly boiled yolk of an egg; 
thin bread and butter (the bread to be one day old). 

Lunch, 11 a.m.: Milk. A thin slice of bread and butter. 

Dinner, 1.30 p.m.: Beef tea, or small piece of minced roast beef 
or mutton, devoid of gristle. One well-mashed potato, moistened with 
gravy. Rice and milk. 

Supper, 6 p.m. : Milk. Bread and butter. 

For drink: Boiled or filtered water. 

DIET FOR A CHILD AGED ONE YEAR (FIVE MEALS A DAY). 

First meal, 7 a.m.: 2 teaspoonfuls of grated flour-ball (prepared 
as directed below) in \ pint of milk. 

Second meal, 10.30 a.m.: J pint of milk with 4 tablespoonfuls 
of lime water. 

Third meal, 2 p.m. : The yolk of one egg, beaten up in 1 teacupful 
of milk. 

Fourth meal, 5.30 p.m. : Same as the first. 

Fifth meal, 11 p.m.: Same as the second. 

Flour-ball is to be made by taking one pound of good flour — 
unbolted, if possible — tie it up very tightly in a pudding-bag; put it 
in a pot of boiling w T ater early in the morning, and let it boil until 
bedtime, then take it out and let it dry. In the morning, peel off the 
surface and throw away the thin rind of dough, and with a grater, 

1 Practical Therapeutics. 



PATHOLOGICAL FIRST DENTITION 213 

urate down the hard, dry mass into a powder. To use this, take 
from 1 to 2 teaspoonfuls of the powder, rub it down until smooth 
with a tablespoonful of cold milk, and add 1 tumblerful of hot milk, 
stirring it well all the time. 

DIET FOR A CHILD AGED FROM SIX TO TWELVE MONTHS (FIVE 
MEALS A DAY). 

First meal, 7 a.m.: Mellin's Food, 1 tablespoonful; or flour-ball 
grated, 1 or 2 teaspoonfuls (prepared as directed above) ; hot water, 
4 tablespoonfuls; warm milk, enough to make § pint. Dissolve the 
Mellin's Food, or rub down the grated flour-ball in the hot water by 
stirring, then add the milk; mix thoroughly. 

Second meal, 10.30 a.m., and third meal, 2 p.m.: A breakfast- 
cupful of milk, with 4 tablespoonfuls of lime water. 

Fourth meal, 5.30 p.m. : Same as first. 

Fifth meal, 10.30 p.m. : Same as second. 

Treatment of Nervous Conditions. — If nervous reflexes, great 
irritability, or cerebral congestion appear, attention should be 
directed to the condition of the bowels and the teeth. 

If constipation or diarrhea exist, a* cathartic is given and the gums 
are lanced. A cerebral sedative is to be prescribed. 

R — Chloralis hydratis . . . . . . . . . . . gr. ij 

Sodii bromidi gr. v 

Aquae menthee piperita? f3ij — M. 

Sig. — Per orem. One dose; enlarge formula for repetition as needed. 

If convulsions be threatened, the clothing should be loosened and 
cool applications made to the head. 

If the child be in convulsions, it should be immersed to the waist 
in water as hot as can be borne, to which has been added 2 table- 
spoonfuls of common mustard flour, and cool water poured over its 
head, when, as a rule, the symptcms promptly subside. Chloroform, 
which children endure well, may be administered. 

After immersion, a rectal injection of 1 dram of glycerin or a 
glycerin suppository will usually cause a free stool. A cerebral 
sedative should be administered. 

R — Chloralis hydratis gr. ij 

Sodii bromidi gr. v 

Starch paste gij — M. 

, Sig. — To be administered per rectum. (Atkinson.) 

It is well also to administer a cathartic, to unload the intestines of 
irritating substances possibly present. 



214 DENTITION 

After sleep, if appearances indicating dental irritation be observed, 
gum lancing is practised. It is wise that this operation be thus 
deferred, as convulsions may be precipitated by the act of lancing 
when the nervous system of the child is overexcited. The removal of 
intestinal irritants, by a cathartic given per orem is also in order, 
before lancing. 

It has been repeatedly noted that when evidence of marked 
cerebrospinal irritation is present, for which no probable source can 
be assigned, and an examination of the gums shows no apparent local 
disturbance, yet if it be at a period when one or more teeth are in 
process of eruption, but are still covered or bound down by gum 
tissue, if gum lancing be practised, relief is immediate and the lancing 
may even avert a threatened attack of eclampsia. It is presumed that 
these are cases of pulp irritation, in which a failure of resorption of 
tissue in advance of the tooth crown has caused pressure upon the 
pulp forming the root end. 

CONSTITUTIONAL STATES MODIFYING DENTITION. 

Children who are the victims of hereditary syphilis, usually cut 
their teeth very early; the alveolar process being in many cases 
insufficient. Cases are recorded where children have been born with 
crowns of teeth visible upon the gum, there being no evidence of root 
formation, the crowns being loosely held to the gum by fibrous 
tissue. It is necessary to remove these loose crowns, to permit the 
infant to suckle. Children affected with rachitis have the process 
of eruption much delayed. It is seen, therefore, that the presence of 
loose crowns of teeth is a condition pointing to, though by no means 
diagnostic of, hereditary syphilis. Long-delayed eruption of teeth 
should prompt a search for further indications of rachitis. Particu- 
larly in children in whom a history of hereditary syphilis is obtainable, 
the process of dentition may be accompanied by rapid and frequently 
widespread breaking down of the soft tissues, over and about erupting 
teeth. Local measures of treatment seem to be of but little avail, 
except that antiseptic treatment undoubtedly prevents complications 
from extraneous infection. 

In children classified indefinitely as strumous, which may mean the 
children of syphilitic or tuberculous parents, or those with no such 
history whose surroundings are of the most unhygienic kind, the 
process of dentition may not only have an untoward course, but 
phagedenic ulcerations may occur. It is usually in the degree of a 
child's debility, either inherited or acquired through improper care, 
that dentition assumes morbid features. The treatment of such cases 



THE SECOXD l)E.\TIT/().\ 215 

must be directed to raising the health standard. As local therapeusis, 
do measures seem more effective than the sprays of hydrogen dioxid 
first; next, potassium chlorate, and, if conditions indicate it, sprays of 
dilute listerine, which is stimulant, antiseptic, and slightly astringent. 

Infantile Scurvy. — Cases are reported in which the improper 
feeding of children has been followed by evidences of scorbutus. It 
occurs usually in bottle-fed babies confined to patent foods, the 
nutritive element being lacking. The gums become tumid, and 
hemorrhagic extravasations occur in their substance; the periosteum 
is stripped from the margins of the alveolar walls, the soft tissues 
hanging in discolored, pendulous masses about and beyond the teeth 
if any be erupted. 

The child is peevish, listless, and feeble. There is apparent pain 
in the limbs. 1 The urine may be bloody even, as a first sign. 

The treatment is largely systemic, and consists of using fresh cow's 
milk modified to conform to human milk, and in the administration 
of fresh lemon juice, preferably boiled, allowed to settle, and the 
supernatant fluid used, 2 or orange juice is also used. 

The mouth should be sprayed with sedative antiseptics, such as 
potassium chlorate in hydrogen dioxid. (See p. 203.) 



THE SECOND DENTITION. 

By reference to Fig. 115, it will be seen that at six and one-half years 
of age, the twenty temporary teeth are still all in position, and that 
taking their places in the line of the arch, are the four permanent first 
molars, the roots of which are still incomplete. 

These molars do not replace any temporary teeth, but during the 
"change" support the jaws with the assistance of the temporary 
molars until the permanent incisors are fully erupted, and with the 
aid of the incisors, until the bicuspids come into occlusion. Their 
office as jaw props and organs of mastication during the change is, 
therefore, very important. Of their later function, more will be said 
farther on. 

At six and one-half years, the crowns of the permanent incisors 
lie in the relations shown, with the temporary central roots resorbed 
and the lateral root partly so. Their crowns are practically complete, 
but the roots are unformed. 

.The cuspid crown in its crypt, lies well above and lingual to the 
unresorbed temporary cuspid root. The roots of the first and second 

1 Hare. * Ibid. 



216 DENTITION 

temporary molars, a trifle resorbed upon the inner side, embrace the 
formed crowns of the first and second bicuspids. 

In their crypts back of the first molars, lie the forming crowns of 
the second permanent molars. The third molars are not in evidence 
in the illustration, but their development is in progress. 

It will be seen that the permanent central and lateral incisors 
replace the temporary central and lateral incisors, the permanent 
cuspid the temporary cuspid, and the first and second bicuspids the 
first and second temporary molars, respectively. 

From this age to adult age, as previously, the jaw undergoes constant 
change, enlarges by constant resorptions and depositions of bone, and 
changes its contour to conform to the changes occurring throughout 
the body, and to accommodate the permanent teeth, which are in 
general terms larger and more numerous than the temporary teeth. 

It may be said that the alveolar process built about the roots of 
temporary teeth and the roots of the temporary teeth are all resorbed 
during the replacement of the latter, and that when the crowns of 
the permanent teeth are fully erupted, new alveolar process is built 
up about their roots. Any subsequent change in the position of the 
permanent teeth is accompanied by an alteration in the alveolar pro- 
cess, and after extraction the latter is resorbed, but upon an implan- 
tation (w r hich see) being done, new process will form. Its dependence 
upon the teeth is, therefore, evident. 

The following table gives the approximate ages for the eruption 
of the permanent teeth : 

First molars 5| to 7 years 

Central incisors 7 to 8 years 

Lateral incisors 8 to 9 years 

First bicuspids 10 to 11 years 

Second bicuspids 11 to 12 years 

Cuspids, the lower usually preceding by a year or more 12 to 14 years 

Second molars 12 to 15 years 

Third molars 16 to 20 years 

and indefinitely beyond 

The Process of Resorption of the Temporary Roots. — After com- 
pletion of formation, the roots of the temporary teeth remain in this 
state but a short time, as their successors are ready to advance to 
their places. 

Comparing the ages at which resorption begins with the ages at 
which it is complete (eruption of permanent teeth) (see Fig. 146), it 
will be noted that approximately three and one-half years are required 
in all cases for the removal of the temporary roots. Therefore, to 
determine the age at which absorption begins, deduct three and one- 
half years from the date of eruption of the corresponding permanent 
tooth. The degree of resorption at any age is shown in the table. 



THE SECOND DENTITION 



217 



At the time the permanent tooth begins its advance, it lies in a 
bony crypt above and lingual to its predecessor, except in the case 



Fig. 140 



* &i 3 re 

1 1 f 1 "-A *A— wfc 9 9 Azzf 

Decalcification of the deciduous teeth. The numbers indicate years. (Peirce.) 



Fig. 147 




Showing the relations of an erupt- 
ing permanent tooth to its deciduous 
predecessor. A, A, A, odontoclasts 
in absorbent organ. 



Fig. 148 




The structure of the absorbent organ, 
showing multinucleated or giant cells 
(odontoclasts). (Tomes.) 

Fig. 149 




Imprisonment of second temporary 
molar; resorption of its roots, with 
absence of second bicuspid. (Skiagraph 
by Custer.) 



of the bicuspids, which lie between the roots of the temporary 
molars (Fig. 112 to 115). 



218 



DENTITION 



Each crypt has its own follicle wall enclosing a permanent tooth 
crown. 

In the follicular wall overlying the crown, appear large multinu- 
cleated cells, the origin of which is unknown, but which by some are 
thought to be transformed osteoblasts, by others leukocytes (Figs. 
147 and 148). The latter is the probable explanation, as analogous 
cells are found about tissues or foreign bodies about to undergo 
resorption anywhere in the body. (See Resorption.) In the par- 
ticular situation under consideration they are called odontoclasts. 
The tissue between the root and crown has by Tomes been given 
the name of the "absorbent organ" (Figs. 147 A, and 148). These 
giant cells have a solvent or digestive function not understood, but 



Fig. 150 



Fig. 151 





Phases of resorption of temporary roots. 
(Skiagraph by Price. 1 ) 



Diagram illustrating the 
relation of a resorbed tem- 
porary root and the perma- 
nent tooth, also the involve- 
ment of the pulp as a part 
of the resorbent organ. 
Resorption of the interior 
of crown of a temporary 
tooth. From actual case. 



which is competent to remove both the organic and inorganic matter 
of cementum and dentin, and evidences of action upon enamel in 
other situations are not wanting. (See Resorption of Enamel.) 
That the solvent is acid, is shown by the evidence of decalcification 
about the area of resorbed enamel of unerupted crowns of some 
permanent teeth. It is a curious fact that no evidence of decalci- 
fication of the permanent crown has been demonstrated to result 
from the proximity of the multinucleated cells in cases of physio- 
logical resorption of roots. In all probability the enamel is pro- 
tected by the presence of Nasmyth's membrane, which Js resistant 



1 Items of Interest, 1901. 



THE SECOND DENTITION 219 

to acids. These cells are probably invited by irritation due to 
pressure of the advancing permanent tooth crown, as the resorption 

is almost always found at the point of approximation of the crown 
with the root, or, in other words, at the pressure point (Fig. 150). 

Cases of resorption of temporary roots without the presence of a 
permanent crown are, however, noted and explained by Tomes 
upon the ground that resorption is a vital act independent of the 
pressure exerted (Fig. 149). As resorption of permanent roots, 
however, has often occurred from pressure of the crown of another 
tooth and occurs at the pressure point in physiological resorption, 
localized irritation, even in the absence of a permanent crown, must 
be credited with a large influence in the process. It is to be remem- 
bered also that in the absence of the pressure, resorption often does 
not occur, at least for twenty-five or more years — e. g., when laterals 
are absent and the permanent cuspids erupt to the side of the 
deciduous cuspids (Fig. 153). 

According to Tomes, redeposition of cementum occurs in pre- 
viously resorbed areas upon temporary roots; a fact corresponding 
with effects noted in permanent roots. 

Teeth frequently erupt lingually or labially to their corresponding 
temporary teeth, both remaining in the mouth. It is almost invari- 
ably the rule, upon extraction to find that an oblique resorption has 
occurred, as is shown in the right upper skiagraph in Fig. 150, and 
generally a decided hyperemia is seen in the pulp extending upward 
for perhaps a quarter of an inch. 

Doskow 1 has shown by the prompt loss, by absorption, of a fairly 
firm deciduous cuspid, crowned to bring it up to level and so to 
usefulness, that such an operation is inadvisable because of an inher- 
ent tendency of an absorbent organ to become established. Again, 
a permanent tooth undergoing resorption often remains firm, until 
suddenly the strain becomes too great. 

As the root of the temporary tooth disappears, the pulp continu- 
ously fuses with the absorbent organ, so that when the crown alone 
remains, the pulp is still vital (Figs. 147 and 151). At times, it seems 
to take up the resorbent function and resorbs the crown dentin in 
some cases almost entirely. In one specimen, a circumscribed portion 
of the cementum and of enamel were removed by it, at the point of 
junction. This constituted practically a case of perforation by 
resorption (Fig. 151). The tooth was at first thought to be suffused 
with hemoglobin, as it was of a pink color. After extraction the 
absorbent organ was found as a papilla attached to the gum. At 

1 Dental Cosmos, 1907. 



220 



DENTITION 



times, bay-like excavations in the crown dentin occur (Fig. 209, ])). 
When the root resorption readies the point shown in the central 
incisor in Fig. 115 the temporary tooth is loosened, moves about, and 
annoys the child, who may pick it out, or it is removed by extraction. 
Formation of the Roots of Permanent Teeth. — The extent of root 
development at any age is of great importance in view of canal thera- 
peutics. Incomplete roots present a mechanical difficulty of sealing 
the apex of the canal. The size of the pulp at the apical foramen 
of such teeth contraindicates the use of arsenic, and even pressure 
anesthesia is often unsuccessfully applied. 

Fig. 152 




Absence of upper left lateral incisor, with permanent cuspid in its place; 
temporary cuspids retained. Man, aged twenty-five years. 



The roots are developed in precisely the same manner as in the 
case of the temporary teeth, by the combined deposition of cementum 
by the osteogenetic cells of the follicular wall, which is drawn up on 
the root as a pericementum, and by the odontoblasts of the papilla, 
which is drawn up as a pulp (Fig. 110). 

The extent of development of any of the permanent teeth may be 
seen at a glance by reference to the valuable table of Peirce (Fig. 116). 
So graphically does this table give the desired information that 
explanation becomes unnecessary. 

Irregularities of Second Dentition. — Some temporary teeth may 
be retained long after adult age is reached. The teeth most subject 
to this are the cuspids and second temporary molars. 



THE SECOND DENTITION 



221 



In the case of the cuspids, the permanent cuspid is delayed or 
takes an unusual direction, erupting lingually or lahially, or at times 
being directed into the place normally occupied by the lateral 
incisors, which are wanting, or very rarely, the cuspid erupts pos- 
teriorly to the first bicuspid. At about forty years -of age, the tem- 
porary cuspids may be lost by resorption of their roots, but until 
such time should be retained if usefully filling a space. If in inter- 
ference with proper alignment or eruption of the permanent cuspid, 
they should be extracted. Their late resorption is somewhat patho- 
logical in character, and probably due to or incited by a partial 
resorption of the root end during the descent of the permanent 
cuspid. 

Fig. 153 




Absence of upper lateral incisors and right bicuspid. Retention of temporary cuspids. 

From an adult. 



The late enforced loss of the temporary cuspid indicates the 
advisability of an implantation operation (Fig. 153). 

The molars are retained, as a rule, because of an absence of per- 
manent crowns to cause resorption, although this ma}' occur without 
such pressure (Fig. 149). I have seen a case of an adult lady with 
eight deciduous molars in place. The question of the abnormal de- 
velopment or absence of permanent germs, or of the state of the 
roots of the temporary tooth may be settled by the .r-rays (Figs. 150 
and 154). 

The question of extraction or retention depends upon the diag- 
nosis. A firm temporary tooth should never be extracted simply to 



222 



DENTITION 



Fig. 154 



allow a permanent tooth to erupt unless the presence of a permanent 
tooth in the jaw, as determined by skiagraph or other means, gives 
reasonable inference that the permanent tooth is held back by the 
temporary tooth. In most cases a reasonable delay is advisable. 
A patient of the editor wore a plate for thirteen years because of the 

injudicious extraction of an upper 
temporary cuspid, the permanent 
tooth appearing at twenty-six years 
of age. 

When the retention of temporary 
molars and cuspids occurs, they are 
apt to occupy an occlusal level, lower 
than that of the permanent teeth 
(Fig. 149). They may not be in 
occlusion at all, as was the case with 
the eight molars just referred to. 
This proves the fact that the general 
occlusal level of the permanent teeth 
is farther from the margin of the alveolar process than in the case of 
the temporary teeth. The length of the permanent crowns accounts 
for this. In normal replacement, however, the occlusal level is nearly 
the same for the temporary molars and first permanent molar, at 
least until the change is made by the eruption of the bicuspid. 




Retained temporary molar with bi 
cuspid present. (Skiagraph by E 
Ballard Lodge.) 



Fig. 155 



Fig. 156 





Retained lower temporary molars, bi- 
cuspid absent. (Skiagraph by E. Ballard 
Lodge.) 



Delayed cuspid. (Skiagraph by E. 
Ballard Lodge.) 



The correct placement of these first permanent molars seems to 
determine the correctness of molar occlusion, at least in the mesio- 
distal relation, though they may not occupy their correct bucco- 
lingual positions. Any slight forces disturbing the mesiodistal 
relation, causing the upper first molar to drift anterior to its correct 



THE SECOND DENTITION 



223 



occlusion with the lower molar, will result in an abnormal relation 
of the teeth to those anterior to them and to their antagonists; either 
upper protrusion or upper irregularities will occur. 

If the reverse occur, and the lower molar be placed anteriorly, and 
the upper be placed normally or posterior to its normal position, 
prognathism of the lower teeth ordinarily results. If placed too far 
posteriorly, retrusion of the lower teeth will occur. 

Fig. 157 




> 



/ 



*> 



irru: 

l I u 



Typical occlusion. (Cryer.) 



According to Angle, the misplacement of the permanent teeth 
erupting early causes their inclined planes to direct other teeth from 
normal occlusion, or by permitting contraction of the space normally 
occupied, particularly in the lower jaw, permits the other teeth to 
assume a position in a contracted arch, thus again causing their 
inclined planes to cause contraction in the opposite arch, with a 
consequent displacement, buccolingually, of teeth which would other- 
wise normally align themselves in the arch. Once established, the 
cheek and lip pressure maintains the inharmony (Fig. 162). 

Angle divides all irregularities into three classes, with divisions 
and subdivisions: 



224 



DENTITION 



Class I. — The first molars are correctly occluded mesiodistally, 
the teeth anterior being in malocclusion, though the biscuspids may 
be in correct mesiodistal relation. 

The general characteristic of the class is that shown in Fig. 158. 



Fig.. 15s 




Malocclusion. Class I. (Angle.) 



Class II. — The lower first molars occlude distally to the upper 
first molars, causing retrusion of the low r er jaw. Division I is char- 
acterized by distal occlusion on both sides, the upper arch is narrowed, 
the upper incisors lengthened and protruded. The upper lip is short 
and functionless, while the lower lip is thickened and rests cushion- 
like between the upper and lower incisors, increasing the protrusion 
of the upper and the retrusion of the low r er. There is usually mouth 
breathing, due to some form of nasal obstruction. 

Division I. — The characteristic exists on one side only, the other 
being normal. Mouth breathing is usually associated (Fig. 159). 

Division II. — There is distal occlusion on both sides, but the 
upper incisors are retruded instead of protruded, with crowding in 
the cuspid region. These are associated with normal breathing 
(Fig. 160). 



THE SECOND DENTITION 



095 



Subdivision, Division II. — The characteristic is upon one side 
only, normal breathers. 

(lass III — Division I. — In this class, the lower first molars occlude 
mesially to the upper first molars on both sides, and the lower jaw 
progressively protrudes anteriorly (Fig. 161). 



L59 



PWBiWg^y 468 468 












SffiSwl 1 »-nf 463 468 _Jg| 




^^^^^^^^^wT| i^^^^™ 




r ^— t*—~f~~ r ~^ ^H HP^"-' 




B~ ^S Ws 






4Hh 


I RIOH T I $ M 1 4A% 46g 


*" LEFT 



Malocclusion. Class II. (Angle.) 



Subdivision, Class III. — The mesial occlusion is upon one side 
only, the other being normal, the arches crossing in the region of the 
incisors. 

Angle has formulated the law "that the best balance, the best 
harmony, the best proportions of the mouth in its relations to the 
other features require that there shall be the full complement of 
teeth, and that each tooth shall be made to occupy its normal 
occlusional relations. He also states that the best development of 
the bones of the face and throat, the size and function of its cavities 
are dependent upon the position of the teeth. 

The specific causes inducing malocclusion of the teeth as classi- 
fied above are: 
15 



226 



DENTITION 
Fio. 1G0 




Malocclusion. Class II. Division II. (Angle.) 
Fig. 161 




Malocclusion. Class III. (Angle.) 



THE SECOND DENTITION 



227 



Fig. 162 



1. Premature loss of deciduous teeth prevents the pressure of the 
first molars upon the teeth anterior to them, which mechanically aids 
in the development of the jaws and thus of the space necessary for 
accommodation of the permanent teeth. It 

also allows the first molar to drift forward and 
come into malocclusion, and also to close the 
space occupied by the deciduous tooth, thus 
lessening space for its successor and forcing it 
into buccal or lingual displacement. The same 
is true of loss of approximal tooth contact as 
the result of caries (Fig. 162). 

2. Prolonged retention of deciduous teeth 
may cause a deflection of the temporary suc- 
cessor or prevent its eruption. 

3. Through loss of permanent teeth on that 
side upon which the tooth is extracted, the 

development of the jaw will be prevented and the tooth posterior to 
the space will tend to tip or drift forward into malocclusion. 




Effects of the prema- 
ture loss of a deciduous 
second molar. 



Fig. 163 



Fig. 164 





Case of adenoids. Fig. 163, before operation; Fig. 164, after operation. (Faught.) 



4. Tardy eruption of permanent teeth permits closure of the space 
altogether or in part, and the resistance offered causes a deflec- 
tion of the tardy tooth (Fig. 162). The total absence of certain 
permanent teeth may be placed under this heading. 

5. Supernumerary teeth, by occupying space, also compel the 
normal teeth to take an abnormal position, and, if erupting after 
them, may displace them by constant pressure (Figs. 220 and 250). 



228 



DENTITION 



6. Habits such as thumb and lip sucking or lip biting will move the 
upper anterior teeth outward and the lower anterior teeth inward. 



Fig. 165 



Fig. 166 





Diagrammatic sagittal section, show- Adenoid vegetations. Compare Fig. 

ing relation of anatomical landmarks. 165. (Faught.) 

(Faught.) 

Fig. 167 




Diagrammatic coronal section through head in the region of the first molar, show- 
ing nasal septum, uncinate process, inferior meatus, inferior turbinals, middle ethmoidal 
cells, middle turbinates, and hiatus semilunaris. (Faught.) 



Holding the tongue between the anterior teeth produces infra- 
occlusion of the anterior teeth, while the constantly open mouth per- 
mits supra-occlusion of the molars. 



THE SECOND DENTITION 229 

7. Nasal obstructions occurring in the developing child produce 
mouth breathing, and the opening of the mouth causes contraction 
of the muscles upon the teeth and bones, producing abnormalities 
of the bone of the jaw; the irregularity of Class II (Division I), an 
undeveloped nose and adjacent region of the face. Faught has ably 

Fig. 168 




Hypertrophy of right inferior turbinal, also deflected septum and spur. 
Compare Fig. 167. (Faught.) 




Cystic middle turbinal, hypertrophied inferior turbinals, enlarged middle ethmoidal 
cells, and hypertrophied middle turbinal. Compare Fig. 167. (Faught.) 

illustrated these conditions in Figs. 163 to 171. 1 The consideration of 
malocclusion as a general subject is properly relegated to special 
works, and the reader is referred to Angle's Malocclusion of the Teeth 
and other works on the subject. 

1 Dental Cosmos, 1908, p. 7. 



230 



DENTITION 



| Disorders of the Second Dentition. — The devitalization of the 
pulp of a temporary tooth and proper canal filling delays, but does not 
absolutely prevent, resorption. Chronic abscesses upon such roots 



Fig. 170 



Fig. 171 





Hypertrophied posterior end of inferior 
turbinal. Compare Fig. 165. (Faught.) 



Nasal polypi. Compare Fig. 165. 

(Faught.) 



Fig. 172 




Right. Left. 

Labial aspect of bilateral sequestra apparently due to typhoid fever alone. (Cowper.) 



destroy the absorbent organ, but some pathological resorption may 
occur, as in case of permanent roots (which see) . Pus has an alkaline 
reaction which may neutralize the acid solvent. As a rule, such roots 
are mechanical obstructions to the permanent crowns, which are 



THE SECOND DENTITION 231 

deflected to one side and caused to erupt irregularly; again, the 
temporary root may be bodily pushed aside, its apex pressed against 
the alveolar process and gum tissue, which are resorbed, and the 
necrotic root end is seen extruded through the gum. Extraction is 
indicated. 

When temporary roots are not thus mechanically removed they are 
gradually extruded and decayed, or suppurative processes cause the 
resorption of the alveolar process about them. 

Injudicious retention of temporary teeth may thus cause an irregu- 
larity. On the other hand, premature extraction by permitting the 
approximation of the previously erupted permanent teeth may have 
an equally bad effect upon an erupting tooth (Fig. 162)1 

In anticipation of physiological resorption of temporary roots, all 
temporary teeth should be carefully watched, cleansed, filled, and, if 
necessary, their roots treated so that a normal replacement by the 
permanent teeth may occur. If pronounced disease occur just 
previous to the time for normal replacement, extraction is indicated. 

Early extraction has sometimes caused early eruption of the per- 
manent teeth, e. g., bicuspids at seven years of age. 

It will be recalled that the teeth are an evolution of the dermoid 
system, which fact possesses pathological significance in certain acute, 
specific skin diseases, lit is noted in some cases of the eruptive 
fevers of children, particularly when the child is much debilitated, 
that after the cessation of the acute disease, a necrotic affection of 
the jaw occurs, involving the alveolar bone and its contents. As 
many of these cases occur between the ages of three and seven years, 
the temporary teeth are still in situ; these, with the partially devel- 
oped permanent teeth and the enclosing bone, may be exfoliated. 
The necrotic process may involve but one tooth, or may include 
all of the temporary teeth, their successors, and a large mass of 
bone. 1 The disease with which this necrosis is most frequently 
associated is scarlet fever; 2 it is also found as a sequel of measles 
and smallpox. " The cases prior to exfoliation of the bone, exhibit 
a stripping of the periosteum, apparently beginning about the necks 
of the teeth. A discharge of pus having a fetid odor is present, and 
the soft tissues may be raised from the bone for a variable extent;" 
that is, there is evidence of purulent periostitis. In the course of 
some weeks, six or eight, the necrotic bone and its contents exfoliate. 
Salter observes that the sequestra forming after severe scarlet fever 
are much more extensive than those which form as a sequel of measles/ 

An interesting case of bilateral sequestra of the aveolar process 

1 Salter, Dental Pathology. 2 Ibid. 



232 DENTITION 

due to typhoid fever alone is reported by CowperJ Two sound 
teeth were involved in each sequestrum. (Fig. 172.) 

The administration to children, of mercurials, has caused such a 
loss of teeth and process. I have seen a sequestrum containing three 
undecayed teeth attributed to this cause, and others have been 
reported. In these cases the parts should be kept as aseptic as 
possible by means of hydrogen dioxid and the compound tincture 
of capsicum and myrrh (enough to cloud a glass of water), used as a 
stimulant mouth wash. 2 When loose, the sequestrum should be 
removed. The parts heal by granulation, if due attention be paid 
to the general physical welfare of the child. 

Eruption of the Molars. — The first permanent molars rarely 
produce more than slight rheumatic pains. The gum irritation 
may be relieved by an X-incision, or at times by the application 
of phenol-sodique and laudanum, equal parts, or phenol camphor, 
with the finger tip. A little alcohol or dilute tincture of iodin serves 
almost equally well. 

As some time may elapse between eruption and occlusion, the first 
molars do not receive a proper friction. Associated frequently with 
carious temporary teeth, they are frequently decayed in their sulci 
and fissures; to prevent this it has been recommended that oxy- 
phosphate of zinc be placed over these fissures without previous 
excavation. 3 The oxyphosphate of zinc or copper may also be thus 
used in third molars which are even more liable to dental caries. 

The lower second molars may cause some irritation owing to an 
insufficient development of the jaw at the angle, leaving an inade- 
quate accommodation for the crown. At about nine years of age 
the second molar occupies the angle of the jaw in much the same 
position as shown in Fig. Ill for the third molar. If held back, a 
pathological condition equivalent to that occurring in the temporary 
teeth may result; reflexes producing heavy pains about the jaw or 
reflex effects, such as chorea, may be produced. 

Truman 4 has prevented a threatened second attack of this sort by 
deep incisions in the gum over the site of the crown. The presump- 
tion is that such treatment relieves the tension upon the pulp under- 
lying the developing root. 

Kirk 5 calls attention to the liability of chorea to be associated with 
reflexes from the dental region at from four to nine years of age, and 
cites a case from the practice of C. N. Peirce in which choreic mani- 
festations were permanently relieved by the removal of a deciduous 

1 Dental Cosmos, 1909, p. 765. 2 Garretson, A System of Oral Surgery. 

3 L. Ashley Faught. 4 International Dental Journal, 1899. 

5 Dental Cosmos, 1905. 



THE SECOND DENTITION 



233 



molar interfering with the eruption of its permanent successor, the 
bicuspid. lie also cites a case of repeated hysterical manifestations, 
following nervous irritability due to each replacement of a deciduous 
tooth by its successor. Flagg cured a case of chorea in a boy, by 
the extraction of four teeth from a very crowded arch. 1 

The third molars frequently induce pathological conditions. 

The upper third molar, meeting in its descent the roots of the 
second molar, may be united to it by hypercementosis — the condition 
of concrescence (which see) ; escaping this, it may meet a dense palato- 
alveolar plate of bone at the tuberosity and be deflected buccally 
through the thinner buccal plate of bone, so that its occlusal face 
presents cheekward (Fig. 173). Its occlusal face may present more 
posteriorly or more anteriorly. Here retained food collects about 
it and caries occurs, or a suppurative inflammation of the cheek 
or free gum margin may occur. For this condition sterilization, free 



Fig. 173 



Fig. 174 





Abnormal eruption of the upper third 
molar. 



Partial eruption and impaction of third 
molar. (Skiagraph by Custer.) 



incision of the gum margin, and subsequent asepsis maintained by 
antiseptic sprays will reduce the inflammation, which, however, is 
apt to recur at intervals. If the cheek be irritated or the position of 
the tooth permanently fixed, only traction of the tooth into a correct 
position, grinding away of the sharp cusps, or extraction will alle- 
viate the condition. The extraction of such a tooth is little loss to the 
individual. A bit of cotton saturated with a mild antiseptic may 
be placed between the tooth and cheek for a time after grinding. 
The possibility of concrescence in such a case, as shown in Fig. 173, 
must be considered when extraction is intended. Individual motion 
is diagnostic of separate teeth, and is readily induced, when the 
crowns are together, by pressing a strong, thin, flat-bladed instru- 
ment between the teeth and turning it. The teeth are seen to move 
apart. 

1 Private communication. 



234 DENTITION 

The pressure of an erupting third molar upon the second molar 
may cause neuralgic pains, and at times the teeth in general, as far 
forward as the central incisor, may seem to loosen up and become 
tender to touch and again become comfortable and tight. These 
symptoms may be repeated apparently in consonance with the efforts 
at eruption. This pressure also causes irregularities of alignment 
or breaks up an orthodontia. Their extraction for this reason is 
sometimes indicated. 

Owing to insufficient development at the angle of the jaw, it is 
almost the rule that the eruption of the lower third molar is attended 
with some degree of discomfort due to gum and bone irritation, and, 
possibly, to pressure on the formative pulp (Fig. 111). 

For some months prior to eruption, heavy, gnawing, rheumatic 
pains may be indefinitely located about the jaw and ear of the 
affected side. The muscles of mastication become stiff and may 
contract spasmodically, simulating trismus. These symptoms, if 
severe, may be relieved by deep X-incisions in the gum; or, if mild, 
by the application of non-discoloring rubefacients or sedatives to 
the outside of the face, over the affected parts. The massage of the 
parts affords some relief. Flagg recommended the following: 

|2 ~§ — Tinct. opii, 

Tinct. aconiti, 

Chloroformi p. aeq. — M. 

Sig. — To be rubbed on the outside of the face. 

Or, 

1$ — Aconitinse gr. j 

Cerati simplicis 5j — M. 

Sig. — To be well spatulated. To be distended with oil of cloves or phenol 
camphor and gently rubbed on the outside of the face, the mouth and eyes to be 
particularly avoided. 

Or, when the aconitine fails to produce relief: 

T£ — Veratrinse gr. xx 

Cerati simplicis gj — M. 

Sig. — To be used in the same manner as the aconitine. 

As the tooth advances, the symptoms may become progressively 
severe. The gum may become inflamed, swollen, and be masticated 
upon, the oral pyogenic organisms produce infection, presumably 
finding an entrance at the point proximating the second molar. The 
patient suffers from the pain and inability to masticate and swallow, 
and becomes nervous, irritable, and debilitated; the breath becomes 
fetid and the salivation excessive. The inflammation extends into 
the contiguous tissue's, and pus may form, extending into them; 
swelling may occur in the adjacent glands, parotid, submaxillary, etc. 



THE SECOND DENTITION 235 

It may also extend to the tonsil or pharynx. All mastication is pre- 
vented, fever is present, and the patient prostrated; septicemia and 
death may follow. 1 Reflex pains may occur. Brown 2 relates a case 
of noma which developed from an infection in this location. The 
gangrenous condition extended to the lungs. Death ensued. 

Results similar to these may occur when the crown is partly 
erupted, being covered at its distal portion by a curtain of gum 
which may be ulcerated upon its under surface. This curtain of 
gum may be thin and stretched, or project rather rigidly over the 
tooth without stretching, as though attached to it. 

In these latter cases the pus, as a rule, finds egress, but occasionally 
it burrows into the pocket between the tooth and contiguous tissue, 
causing much inflammation or pus formation. When gum pockets 
remain about teeth, food may ferment in them and cause deep pus 
formations which may result in Ludwig's angina, a frequently fatal 
disease. (See Ludwig's Angina.) 

Treatment. — The treatment depends upon the stage to which the 
inflammation has advanced. 

If the patient be able to partly open the mouth, the part may be 
sterilized by spraying it with a germicide such as a 1 to 2000 solution 
of mercuric chloride in hydrogen dioxid [or hot carbolized water, 
followed by application of tincture of iodin. (Brown.)] Following 
this an injection of novocain solution is made into the flap of tissue, 
and the gum completely removed from over the face of the crown, 
or, if feasible, any pocket wall cut away. 

To accomplish this, a deep linear cut is made with a sharp bistoury, 
extending from the distolingual to the mesolingual angle of the 
crown. A similar cut is made from the distobuccal to the meso- 
buccal angle. If not already free, the gum is divided at its mesial 
contact with the distal surface of the second molar. The block is 
now penetrated by a tenaculum, drawn tense, and the final cut made 
at the distal border with decidedly curved gum scissors. Less 
cutting is required in some cases. A special gum guillotine is 
obtainable, which practically bites out a piece of the gum flap. The 
electric cautery may be used to burn away the gum tissue (Fig. 175). 

The hydrogen dioxid spray should be again applied to remove any 
possible pus germs present, and should be repeated at intervals of 
about two hours. Tincture of iodin, diluted about one-half with 
alcohol, may be applied every few hours, by means of cotton wound 
on«an applicator or tooth pick, and exerts a germicidal effect. A 
neglect of this simple precaution gave the editor a week of personal 

1 Flagg, and occasional reports. 2 Dental Cosmos, 1908, p. 5. 



236 



DENTITION 



discomfort and inability to masticate, after the removal of a trifling 
and apparently non-inflamed flap of gum. A cold eompress should 
be recommended for the angle of the jaw, if deemed advisable. 
Magnesium sulphate as a derivative may be used with advantage. 

Fig. 175 




Ash's gum guillotine. 

If the patient be confined to his bed and unable to open the jaws, 
a more difficult operation presents. The first object should be to 
reduce the intensity of the inflammatory symptoms. This is accom- 
plished by the removal of the gum block as above, if the mouth can 
be opened sufficiently. Anesthesia may be resorted to, after oral 
sterilization, for the purpose. A jaw separator is introduced, and 

Fig. 176 




Gum scissors. 



operated until sufficient space is gained and the cuts made. If no 
more be possible at the first visit, the lingual and buccal linear cuts 
should be made to insure free bloodletting, which may be increased 
by syringing forcibly with lukewarm water, the position of the 
patient being such that gravity favors its flowing out of the mouth. 
Cold compresses are to be placed over the angle of the jaw and 
magnesium sulphate and the hot pediluvium administered as deriva- 



THE SECOND DENTITION 237 

tives. Cataplasma kaolini, a compound of kaolin (Chinese clay), 
boric acid, methyl salicylate, glycerin, and small quantities of thymol 
and oil of peppermint, 1 are useful, applied in quantity to the face, 
externally. The antiseptic sprays are to be used as before directed. 

If, in addition, local massage or electric heat and massage over the 
angle of the jaw be practised, the swelling and muscular hardness 
usually disappear in a few days. It is well to then remove the 
entire block of gum to prevent reinfection. There can be no ques- 
tion that complete anesthesia and thorough gum block removal, at 
the first visit, is the most advisable surgery. (See Apical Abscess, 
third stage.) 

If the third molar be correctly placed, its eruption, as a rule, 
proceeds uninterruptedly from this point, though it may never be 
entirely free from some degree of overlapping by the gum tissue, 
owing to arrest of eruption by the occlusion of the more advanced 
upper third molar. Pockets are thus formed which favor food 
retention, which, undergoing fermentation, may either cause ulcera- 
tion of the soft parts, or caries of the distal and distobuccal surfaces 
of the tooth. 

Grinding the occlusal face of the upper molar may assist eruption of 
the lower. The gum flap should be anesthetized and removed by the 
thermocautery; or if inflamed, be sprayed with hydrogen dioxid, and 
a pellet of cotton saturated with eugenol introduced for a short time. 

More marked malposition may cause difficulty of eruption, 
necessitating the extraction of the third molar or even of the second 
molar. In some cases it may be better to also extract the upper 
third molar, as it will probably elongate in time and allow food to 
pack into the interspace mesial to it. A presentation of the occlusal 
face of the third molar to the distal surface of the second molar is a 
common form of malposition. 

If very deep seated, the third molar may at times be diagnosticated 
in this position by passing an explorer or thin right-angled blade 
down the distal surface of the second molar, or by means of a deep 
incision with a bistoury or exploring needle. Failing this, or prefer- 
ably, replacing it, the .r-rays are a very valuable means of diagnosis. 

In this situation, pathological resorption of the root of the second 
molar may result, and irritation of its pulp be added as a compli- 
cation. In this case the second molar must be extracted. (See 
Malposition.) 

A more common form of presentation exhibits the distal surface 
of the crown above the gum and the meso-occlusal angle locked 

1 Antiphlogistin is the proprietary equivalent. 



238 DENTITION 

beneath the cervix of the second molar (Fig. 174). Caries is not in- 
frequently induced by the retention of food. The third molar may be 
removed by an operation involving the surgical removal of a portion 
of the base of the coronoid process, followed by extraction. The pulp 
of the third molar may be devitalized by arsenic applied and sealed 
in a pit, drilled in its distal surface. After death of a portion of the 
pulp, the pit may be made to perforate the crown from side to side,, 
and then a dentate fissure bur mounted in the right-angle handpiece, 
or a disk, may be used to saw off the occlusal half of the crown. In 
the space thus gained, and between the second and third molars, a 
wedge of sea-tangle may be neatly fitted; its swelling causes mutual 
separation, which loosens the third molar somewhat, by the process 
of resorption. It should now be quite readily extracted by appro- 
priate movements. 

Cryer recommends the removal of the occlusal section of the 
crown of the third molar by means of a carborundum disk, and the 
removal of the tooth by means of forceps or elevators. Extraction 
in such a case must be carefully done. The use of the elevator is 
dangerous, unless laterally applied, as there is danger of fracture of 
the ramus, which has occurred. (Schamberg.) 

The loss of a second molar may be for other reasons necessary, 
but such a loss in the last case described is equivalent to a loss of 
two teeth, as the third molar will be of little value. 



CHAPTER VIII. 

MALFORMATIONS AND MALPOSITIONS OF THE 

TEETH. 

Abnormalities of the teeth are found associated with position, 
size, form, and structure. Aberrations in form, structure, and size 
are included under the head of malformations of the teeth; aberra- 
tions of position are discussed under the head of malpositions of the 
teeth. The particular section of dentistry relating to malpositions 
of the teeth is by general consent made a special department of 
operative dentistry, that of orthodontia; but many of the phases 
of the subject are of great pathological interest, although the thera- 
peutic measures usually demanded are mechanical in character and 
clearly belong to the fields of operative and prosthetic dentistry. 

Malformations of the teeth may be macroscopic or visible to the 
naked eye, or microscopic, requiring special preparation for obser- 
vation under the microscope. 

The causes of imperfectly formed enamel or teeth must be sought 
by study of the conditions preceding their development. That modi- 
fications of general nutrition must modify tooth development seems 
to be a safe proposition. 

An ill 7 nourished child is apt to have at least poorly organized tooth 
material, while in one that has actually undergone an exanthematous 
disease the tooth form subsequently seen is frequently found to have 
been profoundly modified by the disease. 

MICROSCOPIC MALFORMATIONS. 

Microscopic or histological defects of the teeth may affect any of 
the dental tissues, enamel, dentin, cementum, pulp, or pericementum. 

Enamel. — Defects in enamel structures range from any degree of 
orderliness in the even distribution of globular bodies and cementing 
substance in the tissue, to gross aberrations in formation. The finer 
variations of structure are not easily recognizable. 

Theoretically perfect enamel should show in longitudinal section a 
series of squares of uniform size built into rods, the outlines of 
the squares and rods being marked by lines of cementing substance 
having a refractive index slightly different from that of the squares 

(239) 



240 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

(Fig. 118). While such a structure is perhaps never found, it is 
difficult to draw a line where aberrations from such a standard become 
pathological. An arbitrary standard might be assumed as follows: 
Regard any enamel as pathological, where areas of it differ from its 
general substance to such an extent as to have a decidedly different 
refractive index. A typical form of abnormality is noted in what 
are known as opaque spots in the enamel, areas in which an opaque 
surface exists instead of the normally translucent enamel. 

Fig. 177 



1 ' ' — **=- 


* . . * 




.■ 


%i 






^b&B?*' 




■ 




-^- %- %^ltm ±M 


X 




»„ 




■~0k : - IftjNt 


i • 


-- j^tr- 


■ /m. 




. 4M * 








jafo %*»• 






«& 


- 




m 

w ■ 


41 .; 


% 

1 


i* 


♦ • * ' 




«k% 






\muKwBB^^MmF ^^H^J259HI^HraHK&Biiil 



Portion of a white spot in enamel, showing lack of interprismatic cement substance. 
X 2000. Compare with Fig. 343. (Williams.) 



Opaque Spots in Enamel. — White, brown, and corn-colored opaque 
areas of enamel are frequently seen, surrounded by apparently normal 
enamel. 

Examined without the aid of the microscope they are seen to- 
present a surface as smooth as any enamel, though sometimes slightly 
crenated, but upon this surface being broken up with a bur a chalky, 
granular, whitish material containing at times the yellowish pigment 



MICROSCOPIC MALFORMATIONS 



241 



is seen, sometimes occupying the entire thickness of the enamel. 

These spots, if slight, are sometimes without this granular character, 
while the pigment affects the entire thickness of the enamel. 

Williams submitted the enamel at the borders of such spots to 
microscopic examination, and compared it with enamel in the first 
stages of decay, finding in both a similar appearance, characteristic 
of a lack of, or a loss of interprismatic cement substance (Fig. 177). 

Fig. 178 




Section through human cuspid, showing sulcus and appearance of tissue in its vicinity. 
X 75. (Specimen by Choquet; photograph by Williams.) 



Upon the data derived from his investigations with the develop- 
ment of the enamel, he concluded that these spots are due to a lack 
of such cement substance. This leaves, as the probable substance in 
the spot, unfused globules mingled with some pigment. H. A. Flynn 
concludes that "as about 87 per cent, of children born and raised in 
Colorado Springs have defects in enamel, while in other, close by 
localities these are moderately found, the cause must lie in the lack 
of lime in vegetable matters in that locality and hence in the milk 
of co,ws fed upon them. This lack together with the great demand 
of the developing osseous system for lime causes a deficiency for 
the relatively non-important teeth." 1 In one case of an adult lady, a 



Items of Interest, January, 1910. 



16 



242 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

broad, brown spot was seen on a lower left lateral. There was a 
history of the temporary lateral having been knocked out. 

Enamel formation about the sulci of teeth is frequently faulty; 
owing to an imperfect union of the enamel segments forming the 

Fig. 179 




Section of human molar, showing dentinal fibrillae penetrating enamel. X 600. 

(Williams. 1 ) 



cusps of the teeth, minute fissures exist in the enamel; these are 
most marked in the fissures of molars, as shown in Fig. 178. The 
enamel bounding these fissures has an irregular structure. 

The dentinal fibrillae may penetrate the substance of the enamel 
(Figs. 179 and 184), occupying defined channels in its substance; 

1 For an interesting article illustrating this point see Boedecker, Dental Cosmos, 
1911, p. 1000. 



MICROSCOPIC MALFORMATIONS 



243 



this was formerly regarded as a developmental accident. Caush 1 
claims to have found this to be a normal condition of human enamel, 
and regards these as nutrient spaces. Still later Boedecker has 
found them to frequently occur in enamel (Fig. 184). Andrews 2 
states that 'examination of sections at the junction of formed dentin 
and ameloblasts show fibres span any space formed between them.' 
Evidently there must have occurred a mixture of the elements 
of dentin and enamel, the record showing an interdigitation 

Fig. 180 





Section of human incisor, showing "bands of Retzius" and marked stratification of 
enamel. X 125. (Williams.) 



of papilla (probably odontoblasts) and enamel organ (probably 
ameloblasts). After calcification these odontoblastic fibers are 
caught in the enamel. Von Beust also has experimentally shown 
this (Fig. 109). Such conditions are not to be confounded wnth 
fissures of enamel w T here large lines of faulty calcification or non- 
calcification extend through the thickness of enamel. A portion 
of the enamel may occupy an area within the dentin. This in itself 



1 International Dental Journal, June, 1904. 

2 Dental Cosmos, 1912, p. 49. 



244 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

shows that the enamel and dentin organs can be heterogeneously 
arranged. An odontoma is another evidence. 

Enamel, even normal enamel, is not of uniform composition; were 
it so, it would exhibit, in addition to an orderly arrangement of its 
histological elements, a uniformity in color. So common are differ- 
ences in this direction that the presence of pigment bands must be 
regarded as normal. It is the rule to find enamel traversed by deeply 
pigmented parallel bands, which pass obliquely upward from the 
surface of the dentin to the surface of the enamel. These are termed 
the bands of Retzius; they appear to mark the size of the enamel 
cap at successive periods of its growth (Fig. 180). 

Fig. 181 




Section of enamel from syphilitic tooth, with appearances resembling the lacunae of 
cementum. X 600. (Williams.) 



Stratification and striation of the enamel, as shown by Williams, 
must be regarded as normal physiological records of the mode of 
enamel formation. Kirk has shown that normal enamel shows vari- 
ations in density in the same teeth. 

All of these histological defects represent variations of deposition, 
no doubt due to fluctuation of the nutritive processes of the child at 
the time of tooth formation. Histological records made in the enamel 
are not like those made in other tissues, for there is no certain pro- 
vision through which such defects can be remedied at subsequent 
periods. 



MICROSCOPIC MALFORMATIONS 



245 



Profound nutritive disturbances; such as those attending hereditary 
syphilis in children, affect the structures of the teeth. One of the 
gross results of this disease is a common malformation of the general 
form of the incisors. The hard tissues of such teeth exhibit micro- 
scopic evidences of faulty histology; they are dull and opaque, and 
traversed by irregular bands. Viewed in section, the enamel of such 
teeth is seen to be almost structureless (Fig. 181). Williams found 
that the contents of the large, irregular spaces in this enamel did not 
respond to stains — i. e., did not contain organic matter. Such teeth, 
when not presenting gross malformations, may have a distinct irregu- 

Fig. 182 




Enamel and dentin, human tooth: 1, enamel; 2, dentin; 1, lines of Schreger in 
enamel; 4, brown striae of Retzius. (Probably aggregation of tubes, editor.) (Bromell, 
after Geise.) 

larity of enamel surface. This may even be seen with the naked eye, 
or graphite may be rubbed over the teeth, bringing out the lines. 
Cloud-like markings are also seen in enamel, which are called the 
stripes of Schreger. They run from dentin toward the periphery, 
and are considered by Pickerill to be due to an optical effect pro- 
duced by superimposed prisms 1 (Figs. 182 and 183). j 

There is evidence that other forms of specific dermatitis — scarlet 
fever and measles — which occur at an early age may affect the for- 
mation of enamel. The gross defects attributed to the exanthemata 



1 Pickerill, Dental Cosmos, October, 1913. 



240 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

are irregular pits upon the crowns of, particularly, the incisors (Figs. 
195, etc.), though the cuspids and first molars also suffer. In some 

Fig. 183 




Lines of Schreger in the enamel of a permanent and deciduous tooth (human) . 
Bulge of enamel at cervix of deciduous tooth is shown due to bulging of dentin, not 
to thickness of enamel. (Pickerill.) 

Fig. 184 




Specimen of decalcified adult enamel, showing enamel prism sheaths and lamella (L), 
cut longitudinally. X 500. (Boedecker.) 



MICROSCOPIC MALFORMATIONS 



247 



cases the crowns appear honeycombed. The condition is known as 
hypoplasia of the enamel, and is evidently due to an effect upon the 
enamel organs. The microscopic structure is also affected. There 
is evidence in some specimens (Fig. 194) that the dentin may 
be hypoplastic; the papilla being doubtless affected by the pre- 
vailing systemic malnutrition. The dentin being first developed, 
shows perhaps normal for a distance, then a row of interglobular 
spaces is found, which is evidence that the dentin organ is affected 
by the general disturbance at the same time as the enamel organ. 

Fig. 185 




Section of a bicuspid with its alveolus, showing a pit-like absorption upon the side 
of the root in which the redeposit of the cementum has begun: a, dentin; b, cementum; 
c, peridental membrane; d, bone forming the wall of the alveolus; e, absorbed area of 
cementum. It will be noticed that a new deposit of cementum has begun the filling 
of the area, and that the soft tissue in the area of absorption is of a cellular type. The 
bone also shows the effects of absorption in the cutting away of portions of the ring 
of the Haversian systems at /, while at g the presence of osteoclasts shows that absorp- 
tion is in progress at that point. (Black.) 



Hopewell-Smith 1 describes the enamel developed during rickets as 
faulty, and, in so far as limited observation could determine, con- 
tained numerous spaces probably filled with soft tissue. These 
spaces were in the first-formed portions of the specimens observed. 

Dentin. — Data regarding the finer phases of defective histological 
structure of the dentin are meagre. It has been observed that the 
dentinal tubuli of some teeth are much larger than in others of the 
same age, and, no doubt, future investigations with an improved 
technique directed toward a study of the exact mode of dentin 
formation will exhibit defects more certainly. 

* The chief histological defects noted in dentin are areas of faulty 
or non-calcification, called interglobular spaces (Fig. 186). These 

1 Loc. cit. 



248 MALFORMATIONS, AND MALPOSITIONS OF THE TEETH 



Fig. 186 




Section showing interglobular spaces in dentin of a syphilitic human tooth. (Williams.) 

Fig. 187 



/ 



r^#: 






1 



C'-^l 



Interglobular spaces crossed by dentinal tubes. Prepared by Weil's process. Magnified 
240 times. (Hopewell-Smith.) 



MICROSCOPIC MALFORMATIONS 249 

are most common in the dentin immediately underlying its covering 
tissue; so common in the dentin under the eementum that this 
portion of dentin has been called the stratum granulosum, the 
granular layer of 'Tomes (Fig. 124). In the body of the dentin these 
spaces have a more irregular distribution. 

In wet-ground sections (Hose) the dentinal filaments are seen to 
pursue an unbroken course through these areas. The contents of the 
interglobular spaces react to stains like the sheaths of Neumann; 
that is, they probably contain transitional tissue. These areas 
probably represent, as do defective spots of enamel, periods of 
depressed vitality, or of altered nutrition. In the light of present 
knowledge regarding the subject, they are to be viewed as areas in 
which the calcific process was faulty. The malformations noted in 
connection with the enamel of teeth have their analogues in the 
dentin (Fig. 187; also Fig. 195). 

Fig. 188 




Schreger's lines in dentin. From the ivory of the tusk of a walrus. Prepared by 
grinding. Unstained. X 45. (Hopewell-Smith.) 



Interlobular spaces afford some evidence of the formation of 
dentin by a deposition of globular bodies in a matrix of protoplasmic 
material. The continuation of the tubules through the mass of 
uncalcified contents is evidence of their probable independent for- 
mation by the fibril cells (Fig. 187). 



250 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

Occasionally lines appear in dentin at a common developmental 
level and having a degree of parallelism to the pulp surface. They 
are evidently records of a new period of increment and consist of 
short curves in the tubules. They are called contour lines of Owen, 
also lines of Schreger, in dentin (Figs. 188 and 189). 

Fig. 189 




The same as Fig. 189. X 420. (Hopewell-Smith.) 

Histological malformations of the pulp have not been recorded, the 
normal histology of the organ not being made out with sufficient 
certainty to determine what appearances are to be regarded as 
abnormal. Grosser aberrations, such as those shown in Fig. 137, 
are made out. 

Cementum. — As stated in Chapter VI, the pericementum con- 
tains numbers of multinucleated cells — odontoclasts; and their 
presence is not to be regarded as abnormal. The cementum of the 
roots of teeth may exhibit evidences of former action of these cells 
in excavations of cementum, which, by a subsequent deposition of 
cementum, have become filled. This gives an irregular course to 
the cement lamina? (Fig. 185). These appearances are to be regarded 
as not necessarily pathological, for the following reason: for some 
time (years) subsequent to the eruption of the teeth, developmental 
changes occur in the alveolar bones; depositions (subperiosteal) 
increasing their volume are accompanied by resorption of other 
portions of the bone, such a balance being kept between their pro- 



MACROSCOPIC MALFORMATIONS 251 

cesses that the teeth, although shifting their positions, are kept in 
normal occlusion. 

The cementum may be thickened by additional deposits, as in 
hypercementosis, which is an excess of development classed as 
pathological. 

MACROSCOPIC MALFORMATIONS. 

The teeth may vary from the normal, either as regards size or 
external configuration. 

Variations as to Size. — It is patent to the most casual observer 
that the teeth vary as to size. Comparisons in this direction are 
made by an examination of the upper central incisors. Fig. 191 
shows nearly the extremes of observable sizes; Guilford 1 points out 
that excessively large, central incisor crowns are usually supported 
by abnormally small conical roots. Marked giantism of the central 
incisors usually occurs in pairs, the other teeth being of normal size. 
On the other hand, dental giantism of less degree may involve all 
of the teeth of a denture. The molar teeth are occasionally of 
enormous size, the bicuspids rarely so, and the cuspids next in fre- 
quency to the molars as to the occurrence of giantism. Guilford 
observes that giantism of the cuspid crowns, unlike that of the 
central incisors, is usually accompanied by an increased size of root. 
He mentions the case of a cuspid measuring an inch and one-half 
in length from tip to tip. 

Fig. 190 Fig. 191 





Dwarf Teeth. — Deficiency in size is of more common occurrence 
than excessive size. It appears to occur more frequently with the 
upper third molars and upper lateral incisors than with any other 
teeth. Fig. 192 shows the extremes in size between two perfectly 
formed lower third molars. The stunting of these and of other teeth 
is, however, usually associated with such an aberration of outward 
form, that most dwarf teeth must be considered as abnormal in form 
as well as in size. The writer has seen a supernumerary with crown 
and root together measuring one-eighth inch. 

1 American System of Dentistry, vol. iii. 



252 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

Fig. 192 




Tusk-like permanent central incisors; temporary teeth retained on either side. Female, 

aged twenty- five years. 



Fig. 193 





Conical lateral incisor transformed by porcelain crown. 



Fig. 194 




Hypoplasia of enamel, showing arrested stratification; dentine shows effects of hypo- 
plasia at interglobular spaces (Hopewell-Smith.) 



MACROSCOPIC MALFORMATIONS 253 

A central incisor, or more frequently a lateral incisor, may have 
a conical crown, as shown in Fig. 193. The condition may be double. 

Upper third molars frequently consist of but a single cone, diminu- 
tive in size; at times a crater-like crown is formed by a series of small 
cones about a central pit. 

Treatment. — The Land jacket crown is very useful in modifying 
the cone into a typical tooth form (Fig. 193). 

1 Hypoplasia of the Dental Structures. — By hypoplasia in this con- 
nection is meant an arrested development of any portion of a tooth. 
Necessarily the tooth is deformed. 

Fig. 195 Fig. 196 





Hypoplasia due to eruptive fevers. Hypoplasia of ineisal portion of enamel. 

The term atrophy has been used in this sense, but is better confined 
to a lessening in size after normal development of a part has occurred. 
(See p. 79.) Nutritional disturbances, the exanthemata, and syphilis 
all seem to have a profound influence upon the form of teeth develop- 
ing during the period of active disease, by affecting the cells of 
the formative organs. With the passing of this period, the develop- 
ment of the tooth may proceed in an orderly manner. The fol- 
lowing forms of hypoplasia are known: 

Pitted and Grooved Teeth. — The hypoplasias described under this 
heading may consist of a series of irregular grooves or pittings, the 
crowns having approximately the normal outlines. Of these malfor- 
mations Figs. 197 to 200 are fairly typical. 

Black regards the formation of pits, the simultaneously developed 
zone of enamel being perfect, as due to aberration in development of 
enamel rods, leaving a hole (doubtless a localized effect upon the 
ameloblasts). Histologically the strata of the enamel partly fail of 
deposition at these points (Fig. 195). 

With a history of a case, including the age of the child at the period 
of the disease, if examination be made of the positions of the defects, 
■the age will serve as an indication as to whether there has been any 
connection between the eruptive fever and the dental malformation. 
For example, if enamel pits upon incisors have been caused by an 
eruptive fever between the ages of four and five, they should occupy 



254 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

a part a little above the half-way area of the crown face of a central 
incisor. The lateral will be affected nearer the incisal edge and the 
cuspid still more so; it is evident that the enamel being already 
formed about the incisal edge of the tooth, alterations of nutrition 
could not affect the already formed tissue. (See Fig. 116.) The 
enamel formed after a period of attack may be perfect (Figs. 197 and 
200). 

Fig. 197 Fig. 198 





Showing the front teeth grooved from the alternation of perfectly and imperfectly 
developed portions of enamel. Hypoplasia. (Tomes.) 

Hutchinson's Teeth (Hypoplasia). — During the first few weeks 
after birth, skin eruptions characteristic of hereditary syphilis are 
apt to occur in the contaminated child. At this period the tips of 
the permanent incisors are undergoing development, the first per- 
manent molar having started at the twenty-fifth week of gestation 
(see Fig. 116), and the effect of the syphilitic eruption, during which 

Fig. 199 




Malformations of incisal half of crowns, with cervical half perfect. 
(Model by W. A. Capon.) 



Hypoplasia. 



the protozoon treponema pallidum may be in the enamel organ (or 
there is a severe disturbance of metabolism brought about by the 
infection, according to the preferred view of Stein 1 ), is to cause 
a disturbance of the enamel organ and papilla, which produces a 



Dental Cosmos, July, 1913, p. 693. 



MACROSCOPIC MALFORMATIONS 255 

defective development at this point. Instead of the normal angles 
and flattened curves of the labial surfaces, the incisors may have 

Fig. 200 




Pitted and fringed teeth, some of them carious at the incisal edges. Specimen in 
museum of Philadelphia Dental College. 

Fig. 201 




Hutchinson's teeth. Hypoplasia. Two upper centrals notched and contracted. 
Characteristically undeveloped upper jaw. From an hereditary syphilitic, aged 
twelve years. 

a roughly rounded and stunted appearance. The incisal edge of 
the tooth is narrower than its neck. The enamel at this edge is 
irregularly and badly formed; but there is a semblance of the three 



256 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

enamel tubercles found normally. The middle tubercle, being com- 
posed of defective enamel, is soon lost by abrasion, causing the 
tooth to have a notched appearance (Figs. 201, 202, and 203). Stein 
quotes an old authority as having seen one central notched 
and the other normal. The first permanent molars are often 
exceedingly corrugated and pitted, the pits extending into the 
dentin. These pits often decay, the points are broken or worn away, 
sometimes leaving a discolored, often black surface. (Fig. 204.) 

In an exhaustive treatise upon this subject, Cavallaro 1 has shown 
that the pitted cuspal deformity of the first molars, the notched 
incisors of Hutchinson, and the dystrophic cusps of canines in the 
permanent set, as well as similar effects occurring in the temporary 
set, are the stigmata of hereditary syphilis, either direct or in the 
second generation. He found the treponema pallidum in the dental 
follicles of syphilitic fetuses. 

Fig. 202 Fig. 203 





Syphilitic teeth in upper and lower jaws The teeth of hereditary syphilis at 

as they appear when recently erupted. maturity. 

He calls attention to the possible effect upon the first molar enamel 
(developing before birth) alone, as indicating the cessation of tre- 
ponemal activity, though the incisor enamel (developing after birth) 
is usually affected. The cuspid (developing still later) may not be 
affected; which shows a cessation of germ activity between incisor 
and cuspid development. The dental stigmata may thus occur in 
the absence of the under-developed body and other physical charac- 
teristics of syphilis, though these may also be in evidence, as well as a 
history or evidence of more or less active manifestations of syphilis. 2 

1 Dental Cosmos, 1908. 

2 No matter what conviction a dentist has that these dystrophies are of syphilitic 
origin, he must be cautious regarding the expression of his opinion. Even the thought- 
less leaving of a copy of this volume upon the desk from which it was picked up and 
this chapter seen by a lady patient, produced questions of a very embarrassing character, 
regarding certain defects in her child's teeth. Unfortunately, Cavallaro's investi- 
gations do not take sufficient cognizance of the possible intervention of other exanthe- 
mata, either in the subject or mother; for example, in his Case XX, a girl, aged four- 
teen years, hereditary syphilitic showing transverse grooves in the teeth, the effects 
are attributed to syphilis. The child may easily have had other complications, such 
as measles. Stein excludes rachitis, variola, scarlatina, diphtheria, typhoid and 
rheumatism as very rare possible causes of the hypoplasia. 



MACROSCOPIC MALFORMATIONS 



257 



Stein 1 argues that as the stigmata are bilateral and symmetrical, 
they could not have been produced by causes acting locally, but 
that the general disturbance of metabolism affecting the develop- 
mental organs of the teeth causes interference with the functions 
of such of them as should be actively developing tooth structure. 



Fig. 204 




Semidiagrammatic representation of a systematized hypoplasia of several kinds of 
upper and lower teeth. The general systemic disturbance which must have caused 
these stigmata, commenced about the twenty-fifth week of intra-uterine life and con- 
tinued up to about the fourth month after birth. (The third molars omitted.) 
(Stein.) 



While to syphilis, may now be accredited much of the pittings upon 
teeth, the history of an attack of one of the exanthemata, such as 
scarlet fever or measles, at a certain age corresponding to the devel- 
opment of the particular part of the tooth which has undergone 
hyperplasia makes it rational to accredit the effect to such exanthema. 
Measles often causes characteristic eruptions in the mucous mem- 
brane of the mouth and pharynx, and could easily affect the dental 
follicle. If the disease and the effect do not correspond chronologic- 
ally they should not be related. Syphilis is in a way, an exanthem- 
atous disease of chronic nature. 

In hereditary syphilitics, Cavallaro found the following dental 
stigmata: Hypoplastic defects of systematic character with predi- 
lection for the central incisor forming the notched incisor or Hutchin- 
son's tooth, and also cuspal defects, white sulci, white marks, delay 



Dental Cosmos, July, 1913, p. 695. 



17. 



258 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

of development and eruption, dental infantilism, microdontism, 
amorphism, persistence of deciduous teeth, cuspal defects of decidu- 
ous teeth, especially the second molar, anomalies of structure, 
shape, number, direction, arrangement, and color, vulnerability of 
the dental system, ectopia, total or partial absence of teeth, wearing 
away, premature caries, premature loss of teeth, space between teeth, 
diastema. Also the following maxillary stigmata: malocclusion, 
defective articulation of the dental arches, prognathism, ogival 
palate and cleft palate. 

Fig. 205 




Hutchinson's teeth, cuspal atrophy of canines and molars. Multiple sulciform erosions. 

Diastema. (Cavallaro.) 

Stein offers the following perhaps more clearly expressed classi- 
fication : 

"1. Multiple disseminated stigmata of the teeth, both in the 
maxilla and the mandible. 

2. Symmetrical stigmata here and there upon homologous teeth. 

3. Systematized stigmata at the same level on teeth of the same 
kind, but at a different level on different kinds of teeth. 

The most characteristic stigmata of the teeth of heredosyphilis 
are: 

1. Hypoplasia of the four first molars. 

2. A systematized hypoplasia upon the several upper and lower 
teeth. 

3. Hutchinson's teeth. Microdontism and non-replacement of 
deciduous teeth due to arrested development of the permanent 
successors are regarded by Stein as stigmata." 

Black 1 states that any malnutrition, even a burn, typhoid fever, 
a spasm, etc., may mark teeth as a nail may be grooved. He claims 
to have seen Hutchinson's 2 teeth without history of taint. 

1 Dental Review, 1906. 2 Dental Digest, 1904. 



MACROSCOPIC MALFORMATIONS 259 

As it ordinarily causes embarrassment to question dental patients 
regarding syphillis, the Wassermann and luetin reactions may be 
resorted to if a diagnosis be needed. 

Stein states that the Wassermann may be positive or negative 
in heredosyphilis. 

The point at which the arrested development would occur, is that 
part under development at the time the nutritional or infective dis- 
turbance occurs. When several developing teeth are attacked, the 
centrals are marked nearer the neck than laterals, and these nearer 
than cuspids. The first molars are often occlusally defective, as well 
as incisors, and sometimes the incisors have only white or brown 
spots instead of the incisal notch; bicuspids are only rarely marked. 

A lack of development of the anterior portion of the upper jaw 
has been noted in a number of cases clearly syphilitic (Fig. 201). 
It has been noted that not all syphilitic children present these dental 
appearances; and, again, appearances said to be identical with them 
are observed in children said not to be syphilitic; nevertheless, the 
presence of such teeth is usually regarded as a valuable diagnostic 
sign of hereditary syphilis. The existence of interstitial keratitis 
and of chronic catarrh of the middle ear, in connection with Hutchin- 
son's teeth are held to be positively diagnostic signs of hereditary 
syphilis (Hare). 

Oberwarth, 1 in a synopsis of associate symptoms, mentions 
central deafness, chronic hydrarthrosis of the knee, periostitis of 
the tibia, tumefaction of the spleen and liver, radiating cicatrices of 
the lips, adenopathies, ozena, and deformities of the bridge of the 
nose,- cutaneous gummata, hemoglobinuria, and cerebral phenomena 
as possibilities deduced from a study of his known cases of hereditary 
syphilis. 

In 605 hereditary syphilitics observed by Sidler, Huguenin, and the 
Fourniers, the stigmata averaged as follows: ocular, 50 per cent.; 
dental, 43 per cent.; aural, 16 per cent. 2 

Therapeutics based upon such a diagnosis are followed by better 
results, as a rule, than when the general indication is ignored! The 
boy from whose mouth a model (Fig. 201) was obtained, had inter- 
stitial keratitis in the left eye, chronic nasal catarrh, and a somewhat 
flat development of the nasal bones. 

Tomes favors, and adduces evidence to support the contention of 
Hutchinson, that honeycombed incisal edges of incisors and cuspids 
a*nd occlusal surfaces of first molars are indicative of mercurials 
administered in early childhood. 

1 Review by Dental Cosmos, 1908, p. 179. 2 Cavallaro: Dental Cosmos, 1909. 



260 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

Pitted, grooved, or otherwise malformed teeth may decay some- 
times so badly as to produce a black, slimy appearance almost 
loathsome to view. In other cases surprisingly little caries develops. 

Agenesia of Enamel. — Cases are observed where there has been a 
formative crisis to the extent of having apparently no enamel what- 
ever formed over the occlusal section of the crown, its deposit on 
the remainder of the crown being quite normal (Fig. 196) . 

Fig. 206 




Dentinal tubuli terminating in the spaces of the granular layer. (Tomes.) 

D. B. Freeman 1 records the case of an individual, aged twenty-six 
years, whose teeth anterior to the second molar were entirely devoid 
of enamel. The condition was hereditary; it appeared in both 
brothers and sisters, and could be traced back for three generations. 

Hopewell-Smith 2 claims that teeth apparently devoid of enamel 
have, in all cases examined by him, had attenuated enamel upon 
them. This would also be classified as hypoplasia. 

Black 3 has described the teeth of a man, aged twenty-seven years, 
as having enamel of an opaque, paper-white appearance, as readily 
cut as a slate pencil, and with dentin of ordinary consistence. The 
teeth presented little caries. He also described the temporary teeth 
of a child as all without trace of enamel, the dentin soft, bendable 
in any direction, with production of pain, and penetrable with a 
sharp explorer (agenesia of enamel). 

Treatment. — If slightly pitted, gold or porcelain fillings may be 
introduced. Single pits collect stains which are not removed by the 
brush. It is well to concave these with a small finishing bur, and to 
furnish the patient a sharply pointed stick, for cleansing with tooth 
powder or pumice. In some cases, grinding off the rough incisal 
edge is sufficient; in other cases the teeth may require to be drawn 
down after this procedure, or porcelain inlays may be used to restore 
the incisal edges. In the extremely disagreeable cases above men- 

1 Guilford: American System of Dentistry, vol. iii. 

2 Histology and Patho. Histology of the Teeth. 

3 Dental Cosmos, June, 1908. 



MACROSCOPIC MALFORMATIONS 261 

tioned, some form of crowning must be resorted to. Fig. 207 exhibits 
a restoration of the case shown in Fig. 199. 

Hopewell Smith 1 has observed an entire absence of crowns, not 
due to wear or caries, both on upper and lower teeth, in four 
generations in one family. Therefore, they are cases of extreme 
hereditary agenesia of the crowns. 

Fig. 207 




Same as Fig. 178, with Land jacket crowns placed over anterior teeth. (W. A. Capon.) 

Fusion of Teeth. — Two or more teeth may be united during the 
process of development. The union may occur (1) by the crowns, 
(2) by the roots alone, and (3) by both crowns and roots. 

1. Fused teeth united by the crowns alone have not been shown. 
The nearest approach to it is the case illustrated by Tomes, in which 
two central incisors have fused by union of the crown portions and 
one-fifth of the root portions of the two teeth (Fig. 208). Such 
teeth would have dentin common to both crowns at the point of 
union, the enamel being reflected over the outside of the common 
dentinal mass, according to the scheme shown in the diagram Fig. 
213, B. The pulp may be common to the two teeth in the crown. 
Of course, the root pulps are separate. 

The condition is a record of the fact that prior to dentification the 
papillae and enamel organs of the two teeth have coalesced at some 
point. This must have occurred at an early period, perhaps even 
during the descent of the cords into the jaw. When it is considered 
that the two central incisors are contained in two separate inter- 
maxillary bones, the rarity of such a union and in such a manner 
may be appreciated. I have seen such a union between a right lower 
central and lateral incisor, in the mouth. Recession of the gum 
permitted a view of the cervical conformation. 

1 Dental Cosmos, August, 1913, p. 781. 



202 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

2. Those teeth united by fusion of the roots have a common dentin 
at the point of union, with cementum reflected over that. The pulp 
is common to the two teeth at the point of fusion. 

Fig. 208 Fig. 209 





Lingual view. Labial view. 

Fusion of two permanent upper central incisors by their crowns and a portion of the 

roots. (Tomes.) 

In the specimen shown in Fig. 210 at a there is but one apical 
foramen. In that shown at b and c there is but one foramen for the 
two fused portions of pulp, though the other canals have their usual 
foramina. These cases evidence an accidental coalescence of pulps 
after much independent root formation. 

Fig. 210 




a b c d t 

a, fusion of two molars at the roots — two pulp cavities, one foramen; b, c, fusion of 
supernumerary teeth roofs to buccal roots of upper molars, pulp canal common where 
probes cross; d, view of resorbed root end of two fused temporary teeth; e, concres- 
cence by hypercementosis. 

3. Fusion throughout both crowns and roots have the same charac- 
teristics as the others, combined in the one specimen (Fig. 214), The 
diagram (Fig. 213) shows the scheme for the crown and root. 

Fig. 216 shows specimens of fusion in both the upper and low r er 
jaws. It occurs also with the temporary teeth (Fig. 217). Fig. 



MACROSCOPIC MALFORMATIONS 2G3 

213, .1 shows a very rare condition, the fusion of the temporary 

central, lateral, and cuspid of one side (triple fusion). 



Fit;. 21 I 



Fig. 212 





Attachment of temporary teeth by their 
pericementi. 



Fusion of a supernumerary tooth, with an 
upper third molar. 



Fig. 213 



Fusion is evidently an abnormality of development, dependent 
upon coalescence of formative organs at some point, and is most 
likely to occur where the adjacent tooth follicles have least anatomical 

separation from their fellows. The 
roots of fused temporary teeth are 
resorbed as usual (Fig. 210, d). 

No particular treatment is re- 
quired unless the mass in some 
way causes interference with func- 

Fig. 214 



• A, diagram of a case of triple fusion, 
showing crowns with independent in- 
cisal edges and pulps; but otherwise 
fused into one crown with one pulp; 
B, transverse section of same, showing 
common pulp cavity and common den- 
tin overlaid by enamel (or cementum). 
From a perfect specimen in the editor's 
collection. (Enlarged.) 






Permanent central and lateral incisors of 
the upper jaw, united throughout the whole 
length of the teeth. (Tomes.) 



tion, which is unusual. The teeth having a common pulp, no 
attempt should be made to divide them. 

Fusions are most common between the anterior teeth of each set and 
between the second and third, or third and fourth (supernumerary), 
permanent molars. It has not been noted in bicuspids, presumably 
because these teeth lie in the bifurcations of the temporary molars. 

Concresence of Teeth. — Concresence of teeth is their union after 
the tooth is formed; it is evident, therefore, that the union can onlv 



264 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

be caused by fusion of cementum. This means that during the 
formative and eruptive period, or after eruption, the bony partition 



Fig. 21, 




Geminous upper laterals with common pulp. Practice of Dr. Varney Barnes. 
(Skiagraph by E. Ballard Lodge.) 

between the teeth disappears, and that their pericementi become 
united, receding from the line of compression as cementum is 
deposited between and joining the roots. The united teeth show 
evidences of hypercementosis at points other than the point of union 

Fig. 216 



B 




A, usion of upper geminous, permanent laterals; B, fusion of lower right permanent 
central and lateral incisions. 



(Fig. 210, e, and Fig. 218). At times the roots of the same tooth 
undergo either fusion or concrescence. 



MM 'HOSCOPIC MALFORMA TIONS 



205 



During the eruption of the third molars, particularly the upper, 
temporary lack of space for the eruption of the crown may cause 
resorption of the bone covering the roots of the second molar, and 
fusion of the formative pericementum of the third molar with that 
of the second occurs; a deposition of cementum then binds the teeth 
together, preventing the eruption of the third molar. More than 
two teeth ma}' be thus united. The lower third molar rarely pre- 
sents its roots to those of the second molar; the contrary presentation 
is the rule. 

Fig. 217 




Fusion of'upper temporary teeth. Double fusion of lower'temporary lateral and 

cuspid. 

In at least one case, the crown of the upper third molar was partly 
erupted when concrescence occurred. Retained in this situation, 
the crown decayed away, necessitating extraction; the second molar 
came away with it (see p. 266). The condition also occurs apart 
from the eruptive process. Excessive hypercementosis upon the 
roots of individual teeth may finally result in their union (Fig. 210, e). 

The only treatment required for concrescence is that indicated 
for impaction or hypercementosis (which see) . 

The tough fibrous gum tissue or pericementum has caused two 
temporary teeth to be extracted together at times (Fig. 211). 

Pont cites a case of attachment of a lower first molar distal root 
to the mesial root of the second molar by a strong fibrous ligament, 
2 mm. in diameter, and causing fracture and removal with the first 
molar. There is also sometimes a firm fibrous pericemental attach- 
ment between a tooth and the alveolar process or bone. In one 
case a portion of the antral floor was torn out with the apical tissue. 



200 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 



Fig. 



119 




Fig. 219 



illustrates a remarkable ease of combined fusion, 
concrescence, flexion, and hypercementosis. In this case two 
abnormal third molar crowns were first formed. The roots were 
fused during development, though individual single-pulp canals 
were formed, which joined to form 
one foramen. The lapped condition 
of the roots was due to pulp flexion 
previous to root deposition. The 
carious second molar roots all became 
hypercementosed and probably from 
non-occlusion. As the fused teeth 
erupted, they presented one root to 
one root of the second molar. 

The junction of these occurred as 
the result of formations of cementum 

Fig. 218 




Concrescence. Third upper molar imprisoned 
between the roots of the second molar. 



Case of fusion of two abnormal 
molars and concrescence with the 
root of a right upper second molar 
(restored for illustration.) Pulp 
canals shown in outline. Common 
apical foramen (enlarged.) (From 
author's collection.) 



(concrescence) . The widely open crater-like pit in each crown shows 
the persistence of soft tissue (enamel organ) at that point, or a 
lack of enamel development there. 

Mechanical Union of Teeth. — Teeth upon extraction are occasion- 
ally found united by alveolar bone which is locked between the 
roots of the two or more teeth and prefers to fracture elsewhere. 
Occasionally a sequestrum contains several teeth (Fig. 172). 

Gemination of Teeth (Twin Teeth). — This term has been used by 
Tomes in the sense of union of teeth, but it is perhaps better used 
to designate supplemental teeth of the same class. In twin teeth, 
the enamel organ of a permanent or temporary tooth is duplicated, 
in all probability, two buds arising from the cord or band, as the 
case may be. 

In gemination, one of the teeth formed is, of course, a supernu- 
merary tooth, but in some cases both are typical teeth (Fig. 220). 
The second germ may develop an atypical tooth or one but slightly 



MACROSCOPIC MALFORMATIONS 207 

abnormal in form. The geminous teeth may undergo fusion, as seen 
in Fig. 210, A. 

Duplication of the Pulp Cavity. Hopewell-Smith calls attention 
to a case of an upper permanent central incisor containing two pulp 
cavities in the coronal portion, probably an interrupted gemination. 

Fig. 220 




Double gemination of upper permanent lateral incisiors 



Dilaceration. — By dilaceration is meant a displacement of a formed 
portion of a tooth in such a manner as to change its relative position 
to the soft parts engaged in its development, the development then 
being continued in the new relation. 1 For example, an accident to 
a temporary tooth occurs and the force may displace the partially 
formed permanent crown, altering its relation to the enamel organ 
and papilla engaged in its formation. The balance of the crown 
ma}" be formed in the new situation and be of fairly perfect or of 
imperfect structure (Fig. 221). This is most likely to occur with 
the anterior teeth, especially when a temporary tooth is driven into 
the alveolar process, its root in turn displacing the permanent tooth, 
thus twisting its relation to its formative organs. 

Flexion.— Flexion means the movement of one of the formative 
organs of a tooth away from its normal relation to the hard part it 
is developing. The soft part has its position altered, the hard part 
remaining in correct position. Subsequent formations therefore 
have an abnormal relation to the previously formed portions of the 
tooth. 

As an example of flexion, a portion of the enamel organ of a tooth 
may be displaced and in its new relations may form enamel in an 

1 Tomes. 



208 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 



unusual situation, as, for example, upon the side or neck of the root 
(see enamel nodule) or even in the bifurcation or on the apex of the 
root (Figs. 222 and 225). Again, it is probable that lack of space 
may cause deflection of a pulp engaged in root formation, a curved 
root being the result (Fig. 231). The pericementum (follicle wall) 
moves with the pulp in these cases. 



Fig. 221 



Fig. 222 





BofR 



Pulp hernia and flexion, mesiodistal 
section: E, enamel, distal section in the 
bifurcation of the roots; D, dentin; C, 
C , cementum; PC, pulp cavity; F, large 
apical foramen : B of R, bifurcation of the 
roots. (From a specimen, enlarged.) 



Fig. 223 



Dilaceration. Shows fold in the labial 
enamel and cervical dentin. (After von 
Wunschheim. 1 ) 




Enamel excrescences. (Salter.) 



Unusual Locations of Enamel. — That during development, the enamel 
organ or portions of it, may assume an abnormal relation to the pulp, 
is evidenced by odontomes. Apart from these, there are evidences 
seen in teeth which show that portions of the enamel organ may 
become detached from the main organ, and develop enamel in unusual 
situations. Thus columns of enamel may penetrate the body of the 
dentin. 

A small nodule or cap of enamel overlying dentin, and itself over- 
lapped at the edges by cementum (Fig. 226), may be found upon the 
root of a molar, usually upon the side of an upper third molar at a 

1 G. von Wunschheim: Fracturen, Infraktionen und Knickungen der Zahne. 



MM 'ROSCOPIC MA LFORMA TIONS 



269 



point about one-eighth inch from the cervical margin of the crown 
enamel; but one may be one-half inch distant from the enamel mar- 



FlG. 22 1 



Fig. 22i 





Lower molar with enamel nodule 
connected to the enamel of crown by 
a ridge enamel. 



Five-rooted upper molar, cap of enamel 
on end of one root. 



gin. A thin ridge of enamel sometimes, though not usually, seen 
connecting them, indicates the nodule to have been formed by a 
detached portion of the original enamel organ (Fig. 224). This forma- 



Fig. 226 




Structure of enamel nodule. E, enamel; D, D, dentin. (Hopewell-Smith.) 



tion is known as an enamel nodule. It may occur upon a lower 
molar, though usually found upon the upper molars. Two may 



270 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

exist on opposite sides of a molar, as in a specimen possessed by the 
editor. They may cause neuralgia. (Ottofy.) 

A molar root may have a cap of enamel upon its apex, an evidence 
of extreme displacement, even more than shown in Fig. 225. Some- 
times an enamel ridge runs down the side of a root; sometimes an 
excrescence may be found upon the enamel (Fig. 223). Fig. 222 



Fig. 227 



Fig. 228 



Fig. 229 




Upper molar 
with supplemental 
cusp on lingual 
side. 




Showing talon-like un- 
usual development of 
the cingule on an incisor. 
(From case reported by 
W. H. Mitchell, Dental 
Cosmos, vol. xxxiv.) 




Very large supplemental cusp 
on the buccal surface of upper 
molar. Probably a fused "para- 
molar." 



shows enamel formed in the bifurcation of the roots of a lower 
molar. This enamel nodule has been explained upon the hypothesis 
that the remains of the epithelial root sheath of Hertwig Jiave within 
them the inherent power of forming enamel, which may account 
for enamel on the side or end of a root. As this epithelial root-sheath 



Fig. 230 



Fig. 231 



Fig- 232 





m 

Cuspids with long roots. 




Curved roots. 



Upper cuspid with two roots. 



is probably the trailing remains of the enamel organ left as the 
organ is carried up by the tooth, it is quite likely that larger portions 
of the organ may be detached as above explained. (See Fig. 98.) 

Supplemental Cusps. — Occasionally a tooth has a greater number of 
cusps than usual. The most common form of this condition is a 
supplemental mass attached to the palatal side of the mesopalatine 



MACROSCOPIC MALFORMATIONS 



271 



cone of the upper first molars (Fig. 227). It is more rarely the case 
that a cingule of this sort is noted upon the lower molars. The 
palatal tubercle, the prominence upon the cingule of an upper incisor, 
may be of exaggerated size. In one case (Fig. 228) this develop- 



FiG. 233 



Fig. 234 



Fig. 235 






Short buccal root of a 
molar, otherwise properly 
developed. 



Central incisor with 
short root. 



Five-rooted upper third 
molar. 



Fig. 236 



ment gave the appearance of a talon upon the tooth, a distinct cusp 
segment in itself. Fig. 229 illustrates a marked supplemental cusp 
upon the buccal surface of a molar. A fusion in this location is not 
impossible. (See Fourth Molar.) 

Malformations of Roots. — Differences in regard 
to the size, arrangement, form, and number of 
the roots of teeth are the most common of the 
dental malformations. The roots of teeth may be 
abnormally long (Fig. 230) or abnormally short 
(Figs. 233 and 234). 

The Toots of cuspids may be bifurcated, par- 
ticularly in the lower jaw (Fig. 232). A central 
may have a short supplemental root. (Guil- 
ford 1 ), or sometimes two distinct roots as in 
Fig. 236. 

The upper first bicuspids may have trifurcated 
roots, the extra root usually being on the buccal 
aspect. The upper second bicuspid may be bifur- 
cated; upper molars may have more than three 
roots, the third molar often having four, five, or 
six, and in one case reported, eight roots (Figs. 225 and 235) . In 
some cases upper third molars have but one root with a single, large 
canal, a case of true developmental fusion. In other cases the roots 
are* fused so as to form apparently but one root, while the canal 




Two-rooted upper 
right central incisor. 
(Warren. 2 ) 



American System of Dentistry 
Dental Brief, April, 1913. 



272 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

divisions may exist. This may be fusion or concrescence of roots. 
Lower molars may have three or four distinct roots, but rarely only 
one. 



Fia. 237 



Fig. 233 



Fig. 239 






Fibrous odontome. 
(Garretson, after 
Pierce.) 



Two-rooted lower cuspid. 
Resorption of temporary 
roots. (Skiagraph by E. 
Ballard Lodge.) 



Results of hernia of 
pulp. (Salter.) 



Fig. 240 




Fig. 239 magnified. 



MACROSCOPIC MALFORMATIONS 273 

Abnormalities of root form are of extreme frequency, and are 
probably explained upon the hypothesis of flexion of the root pulp, 
previous to the deposition of the curved portion of root tissue. 

It is impossible to diagnose the forms of roots from the appear- 
ance of the crowns, but a skiagraph will determine their form with 
certainty. It may be said, however, that narrow necks indicate a 
probable divergence of roots, and vice versa. 

An excrescence upon the cementum is known as a cemental nodule. 

Odontomata. — An odontoma is a growth composed of structures of 
which the teeth are composed, but the masses may be so arranged 
as to have no typical form or even resemblance to a tooth. They may 
appear in the arch or may remain embedded in the jaw, where they 
ma}* lie quiescent or may excite cyst formation (Fig. 31), or give rise 
to various morbid reactions, such as tumor formation. 

It has been held by Broca that any of the formative organs of the 
tooth — enamel organ, dentinal papilla, or follicle wall — may undergo 
aberrant development and may thereafter deposit calcific tissue or 
not, as the case may be. If not, soft tumors of the jaw, not dis- 
tinctly dental, may form, though in its complete form such a tumor 
may become a seat of calcific deposition peculiar to the aberrant 
tissue. 

Fig. 241 Fig. 242 





Radicular odontome. (Tomes.) Odontoma. (Garretson.) 

Bland Sutton's classification is usually adopted, and is as follows: 

1. Aberrations of the enamel organ: (a) Epithelial odontomes. 
(6) Calcified epithelial odontomes. 

2. Aberrations of the follicle: (a) Follicular cysts, (b) Fibrous 
odontomes. (c) Cementomata. (d) Compound follicular odontomes. 

3. Aberrations of the papilla : (a) Radicular odontomes. (b) Den- 
tomata. (c) Osteodentomata. (d) Cementomata. 

4. Aberrations of the whole tooth germ (or three formative 
orgajis), composite odontomes. 

The Uncalcified Odontomata: 1. Epithelial odontomata which 
arise by aberrant development of the enamel organ, and remaining 
uncalcified resemble the adenomata. 
18 



274 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

2. Follicular odontomata: (a) The wall of the follicle is distended 
and the cavity is filled with a thick fluid (sometimes pus if infected), 
and contains a portion of imperfectly developed tooth. It is in this 
form really a cyst (Fig. 31). (b) The follicle wall or pericementum 
may thicken so as to form a fibrous capsule about the tooth, suffi- 
ciently resistant to prevent its eruption (Fig. 237). This is called 
a fibrous odontome. 

3. Compound follicular odontomata: The follicle wall thickens 
into a fibrous capsule, and in this may appear fragments of cemen- 
tum, dentin, or imperfectly formed teeth with their enamel, dentin, 
and cementum. 

Fig. 243 




Composite odontome. (Garretson.) 



It is a combination of an uncalcified and calcified form, and might 
easily lead to formation of a cyst containing many teeth or portions 
of teeth. 

The Calcified Odontomata: 1. Epithelial. The enamel organ 
develops aberrantly into a large, possibly multilocular mass, and 
enamel deposition occurs. 

2. The Cementomata: A fibrous odontome forms from the follicle 
wall, then calcifies into laminated ossific material. One from a 
horse, in the Royal Veterinary College, London, weighed seventy 
ounces. It may include one or more teeth. 

3. Radicular Odontomata: The crown may form normally, but 
the dentinal papilla becomes aberrant and develops largely, conveying 
with it the follicle wall. Ceasing to enlarge, cementum and dentin 



MACROSCOPIC MALFORMATIONS 



275 



are deposited somewhat in the ordinary manner, but of somewhat 
aberrant deposition. Pulp hernia comes under this heading and 
acts similarly (Figs. 239, 240, and 241). 

4. Composite Odontomata: The developmental organs, the 
enamel organ, the papilla, and follicle wall are aberrant, hetero- 
geneously arranged, enlarged, and then deposit a composite mass, 
which may be somewhat orderly and tooth-like (Fig. 242), or be 
totally unlike a tooth as in Fig. 244. 

The diagnosis of odontoma, if at all obscure may be made by 
skiagraphy (see Fig. 245). 

Fig. 244 




Composite odontome. (Garretson.) 



Treatment. — The treatment of odontomata is usually that directed 
to their sequels, which consist of enlargements about the jaws with 
more or less inflammation or cyst formation, and, as a rule, involves 
their removal by surgical operation. 

Anomalies of Number. — Although the dental series of man nor- 
mally consists of thirty-two members, cases are frequently observed 
in which the number is less than, or in excess of that number, or there 
is an abnormal number in any particular group of teeth. 

Deficiency. — It is observed with some frequency, that the upper 
lateral incisors never make their appearance, a condition traceable to 
the influence of heredity in some of the instances. In an interesting 
case of three sisters, who all were without upper laterals, a son of one 
of them had them. Unfortunately the history, as to the parents of 
the sisters, was not certain, as they wore artificial teeth. 

When the laterals are absent, the permanent cuspid erupts and 
occupies the lateral incisor space, and thus sometimes fails to cause 
resorption of the root of the temporary cuspid, which persists in the 



276 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

cuspid space (Fig. 153). The lower laterals sometimes, but more 
rarely, fail to appear; are probably never formed (Fig. 247). The 
third molar may never appear, or appear as a peg-like tooth. 

The cuspid often is impacted but is seldom lacking in formation. 
Usually when missing it is to be found by skiagraphy. 

Fig. 245 




Surgical fracture of mandible, with 
photograph of odontoma and molar 
tooth after removal. (Graham.) 



The cases of suppressed teeth, 
next in point of frequency, are 
those of the bicuspid teeth. If 
the corresponding teeth are all 
present in the dental arch, a 
well-founded suspicion of impac- 
tion of the missing tooth may be 
entertained. 
An excessive growth of hair upon the face and body has also been 
associated, in some cases, with a deficiency in number and altera- 
tion in form of the teeth. In other cases no abnormality was notice- 
able. 1 In some cases the hair and other dermal structures may be 
normal and the teeth be quite deficient in number. 

The extreme of suppressed formation is represented in a case 
described by Guilford. 2 



Tomes: Dental Surgery. 



American System of Dentistry, vol. iii. 



MACROSCOPIC MALFORMATIONS 



277 



A patient over fifty years old had never erupted any teeth, tem- 
porary or permanent; the alveolar arches revealed no evidences of 



Fig. 246 




Structure of a composite odontome. (Garretson.) 
Fig. 247 




Absence of both upper and lower laterals in the same mouth. Temporary left upper 

cuspid. 

enclosed teeth, but had the appearance of typical edentulous jaws; 
the alveolar bone itself was but primitive. The case appeared to be 



278 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

sporadically hereditary, a grandparent and an uncle exhibiting a 
like condition. The cases are interesting also because of additional 
evidences of faulty evolution of dermoid structures. In the first 
case cited, no sudoriparous glands appear to have formed, and there 
was but a faint growth of hair on the cranium, and none on the 
face and body. The uncle was hairless and edentulous from birth. 
Guilford found, in other members of the family, an absence of the 
full complement of teeth. 

In an interesting summary, Kjaer 1 quotes Trueswell as knowing 
of a man, aged fifty-four years, having had no permanent teeth, but 
all of his temporary ones, and Fricke as having 3 cases of retention 
of temporary teeth until sixteen, eighteen, and twenty years respec- 

Fig. 248 




Malposition of molar teeth. 

tively, when the permanent teeth appeared, and Linderer as having 
a case of a lady, aged sixty years, who never had any teeth, and a 
case of his own in which the temporary teeth were lost from time to 
time, but no permanent successors appeared, and none could be 
detected by skiagraphy. He attributed the lack to some disturbance 
during fetal life, as the family history did not include such a case. 

Excess. — The possible occurrence of a condition in some respects 
the reverse of the preceding, has been much written of and discussed 
— i. e. y the occurrence of a complete third denture. There can be but 
one conclusion from an examination of all the evidence thus far 
presented, and that is that no clear and well-authenticated cases are 

1 Dental Cosmos, 1907. 



MACROSCOPIC MALFORMATIONS 279 

made out. Isolated cases of the appearance of teeth subsequent to 
the loss of all of the second denture are not infrequent; and, so far 
as clear records can he obtained, are resolvable into cases of the 
eruption of supernumerary or impacted teeth, though sometimes 
a number of teeth are reported erupted. While these cases are, 
at least for the present, to be held as unproved in connection with 
elderly persons, a well-authenticated case of multiple dentition in 
a child is recorded by Catching. 1 Between the sixth and seventh 
month the eruption of one set of teeth was complete; within three 
months all of these had been lost. Between the eleventh and fifteenth 
months another period of dentition occurred, the teeth of this second 
denture being of such faulty^ structure as to crumble away quickly. 
At the age of two and one-half years a third dentition appeared, 
which caused the child such inconvenience that the teeth were 
extracted by the mother. At the age of eleven years a fourth series 
erupted, incomplete through the absence of six teeth. At the age of 
fifteen years these teeth were sound and firm. 

The Fourth Molar. — Very rarely a fully developed fourth molar 
appears in the maxilla. In one case it was impossible to distinguish 
the normal. The third and fourth lay in lingual and buccal relation. 
Less rarely, a less typical molar appears posterior to the third molar. 
This must be very rare in lower molars. A third type of super- 
numerary appears in the maxilla. These are rudimentary, and 
appear upon the buccal side, opposite the approximation of the 
first and second molars or of the second and third molars, or to the 
distal or distolingual of the third molars. Bolk 2 calls the buccal 
supernumerary the "paramolars," and says they are small, two- 
cusped, single rooted, and, if fused, usually unite with the mesio- 
buccal portion of the tooth posterior to it during development. Here 
it forms a supplemental section, "paramolar tubercle" (Fig. 229), 
which may have a distinct " paramolar root" or root indication. Bolk 
accounts for the less frequent appearance of an anterior independent 
paramolar (opposite the approximation of the first and second molars) 
upon the supposition of a more frequent fusion with the second molar, 
and he has found twice as many "paramolar tubercles" in the second 
molar as in the third. The supernumerary posterior of the third 
molar he terms the "distomolar," and finds that when fused, it 
unites with the distolingual section of the third molar. He has noted 
a rare case having both a paramolar and distomolar. He also has 
ndt observed independent paramolars in the mandible, bnt the para- 

1 Southern Dental Journal, October, 1886. 

2 For the many beautiful illustrations enforcing this new conception the reader is 
referred to the article in Dental Cosmos, February, 1914. 



280 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

molar tubercle may occur on the second or third molars, which may 
have a proper "paramolar root." The distomolar in the mandible 
fuses with the distolingual portion of the third lower molar. He 
calls attention to the fact that in the maxilla ; the paramolar appears 
most often as a supernumerary tubercle, while in the mandible it is 
emphasized by a supernumerary root. 

Supernumerary Teeth. — Any teeth in excess of the normal number 
of teeth belonging to any one class are included in the category of 
supernumerary teeth. The number of teeth may possibly not exceed 
thirty-two. Supernumerary teeth appear as simple unmodified 
cones, or as combinations of cones resembling the forms of teeth. 
The conical form is most common. Cases where these peg-like teeth 
appear around the third molars, singly or in number, are numerous. 
Their appearance in any situation is evidence that the normal number 
of dental cords has been exceeded. 

Fig. 249 




The fourth molar (Hartman.) 



Guilford 1 divides supernumerary teeth into those having typical 
anatomical forms and those having atypical forms. 

Supernumerary incisors having typical forms appear in either 
jaw. In the upper jaw, supernumerary centrals and laterals both 
appear, the latter more frequently (Fig. 220). Supernumerary teeth 
may occupy any position relative to the dental arch, but are more 
frequently seen at its lingual side. The compound cone occasionally 

1 American System of Dentistry, vol. iii. 



MACROSCOPIC MALFORMATIONS 281 

appears (Fig. 251). In addition to molars and incisors, supernu- 
merary bicuspids are occasionally found (Fig. 232); supernumerary 

Fig. 250 



Two atypical upper supernumerary teeth displacing the incisors. 

cuspids are very rare, but sometimes a brood of them exists, as many 
as seventeen fairly defined small teeth having been removed from a 
cyst in the location of the cuspid tooth. 1 

Unless supernumerary teeth are a source of offence, FlG - 251 
either through their position or appearance, they 
need not be disturbed. If they are found to be so, 
they should be extracted. 

Malpositions of the Teeth. — A tooth is said to be 
in malposition when it is not in normal relation with 
the dental arch to which it belongs and to its 
antagonizing teeth of the opposing arch. Teeth are The compound 
found in abnormal positions as the result of a variety cone - 

of causes. Some of these operate prior to, during, or 
immediately after eruption; some long after the eruption of the 
teeth, and some because of non-eruption of teeth. (See p. 220, etc.) 

Malpositions which are remediable through the application of 
mechanical force, applied by means of suitable apparatus, belong to 
operative dentistry, as has been stated. They are fully treated of in 
works upon operative dentistry 2 and orthodontia. 3 

1 D. M. Clapp: International Dental Journal, 1900. 

2 American Test-book of Operative Dentistry. 3 Guilford, Angle, and others. 



282 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

The extraction of teeth after they have been erupted, or of their 
predecessors, is one of the most frequent causes of acquired mal- 

Fig. 252 




Case of seven lower bicuspids, two supernumeraries in place and one erupting. This 
patient has two supernumerary upper central incisors displacing the centrals proper, 
yet closely resembling them. 



Fig. 253 



position of the remaining teeth. The teeth move from their original 
positions, the anterior teeth, incisors, laterals, cuspids, and occa- 
sionally the bicuspids, having a tendency to drift posteriorly, some- 
times opening a space between the central in- 
cisors, sufficiently large to create a deformity. 
The molars have a decided natural tendency 
to drift forward, and when the bicuspids are 
removed they tip anteriorly, causing maloc- 
clusion upon their distal cusps and sometimes 
their distobuccal cusps alone, with a further 
tendency to tip forward and sometimes inward 
as well. Separation of the posterior teeth may 
occur, and in any event, the loss of mesial or 
distal support permits fibrous food to be packed 
between the teeth; as they spring slightly apart, 
it is held by their springing together again. 
The lack of occlusion brought about by extrac- 
tion of antagonists permits elongation, and the 
loss of posterior support is apt to bring about labial protrusion or 
abrasion of upper anterior teeth. This effect is produced in youth 




Effects of premature 
loss of permanent first 
molars. 




IMPACTION OF TEETH 283 

when the first molars are lost before the bicuspids are in place (Fig. 
253). The first molars are the keystones of the arches, and determine 
the extent of the formative process which shall occur in the alveolar 
bone posterior to them. They are also the teeth which, correctly 
placed or out of position, determine largely the occlusion of the teeth. 1 

If a temporary tooth be long retained, it is sometimes raised to 
the occlusal level of the other teeth; again, it is sometimes left at its 
original level and occasionally imprisoned between other teeth. The 
sc-rays should be used to determine the presence or absence of the 
permanent tooth germ or resorption of the temporary roots. 

If teeth erupt in malposition, it is held to be wise to correct as 
early as possible, in order to prevent further malposition of other 
teeth. 

Fig. 248 illustrates a case of malposition of molar germs which have 
developed in the incisal region, displacing the incisors. 

Impacted and Encysted Teeth. — The extreme extent of dental 
malposition is reached when the permanent teeth do not erupt at 
all. Instead of presenting in the dental arch, they may be entirely 
embedded in the substance of the bone, either remaining there, with 
or without pathological manifestations, or erupting in some unusual 
situation. In other cases, a distinct cystic tumor forms about the 
enclosed tooth (Fig. 31). The cause of impaction probably lies 
either in a previous malposition of other teeth preventing advance, 
or in an originally malposed tooth germ, or to the development 
of the root while the crown advance is retarded, the expulsive 
force of root formation being lost. In many cases orthodontic 
procedures creating room may permit the descent of the tooth. 

Impacted Lower Third Molars. — By far the most common dental 
impaction is that of the lower third molar. The extent of impaction 
varies from a partial eruption, or partial imprisonment of the tooth by 
its bony surroundings, to its entire imprisonment in any part of the 
ramus. Many of the more severe cases treated under the head of 
pathological dentition, if unrelieved, would be included in the category 
of impacted teeth. 

In Fig. 254 is shown a lower third molar presenting the effects of 
a previous impaction. The irritation caused by the efforts of the 
tooth to disengage itself, or to overcome the resistance to its erup- 
tion, has caused an active formative reaction in the pericementum, 
resulting in an hypertrophy of the cementum. Likewise the pressure 
u'pon the bone causes a condensing osteitis, and the bone becomes 
dense, more obstructive, and less vascular (see p. 144). 

1 Angle. 



284 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

If the distance between the posterior surface of the second molar 
and the columns of the coronoid process be very short, it is evident 

Fig. 254 




Right hal iof lower jaw, showing an impacted third molar. (Cryer.) 
Fig. 255 




Inner side of left half of same lower jaw. (Cryer.) 



that upward eruption is impossible, so that the tooth may assume 
any direction of movement, the most common being forward, the 



IMPACTION OF TEETH 



285 



axis of the tooth changing its position until the tooth may lie in a 
horizontal position or even become inverted. 



Fig. 25G 




Impaction of lower third molar. Resportion of root of second molar and impingement 
of root upon inferior dental canal, which is deflected out of its course. (Cryer.) 

Fig. 255 is taken from the same jaw as Fig. 254, but shows the 
opposite side; the impaction is pronounced. Fig. 256 shows another 
case with different anatomical surroundings. In the first case there 
were evidences, both in the tooth, in its bony surroundings, and in 
the external cortical bone, of the results of the irritation produced 
by the efforts at eruption. The cementum was thickened; the outer 
folliculaT wall, the tissue designed to form the alveolar periosteum, 



Fig. 



Fig. 258 





Impacted lower third molar beneath gum. 
Second molar tipped forward. (Skiagraph 
by E. Ballard Lodge.) 



Impacted cuspid. (Skiagraph by E. 
Ballard Lodge.) 



had exercised its formative osteogenetic function, and a capsule of 
bone had formed about the tooth; it lay in a bony chamber. The 



286 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

pressure exerted upon the distal wall of the second molar had resulted 
in a pressure resorption of its root until the pulp chamber was 

Fig. 259 




Impacted bicuspid. (Skiagraph by E. Ballard Lodge.) 

encroached upon. These were both postmortem cases, and no records 
of their clinical histories were obtainable. The symptoms produced 

Fig. 260 




Same as shown in Fig. 234, with tooth removed. (Cryer.) 



could only be surmised by the nature of the anatomical relations 
and the pathological evidences. There may have been a prolonged 



IMPACTION OF TEETH 



287 



but mild periostitis, probably a continued pulp irritation; and in the 
last, neuralgia of any grade of severity. The pressure upon nerves 



Fig. 261 




Wisdom teeth embedded in the rami of the lower jaw. (Tomes.) 




of the inferior dental canal would account for neuralgia or mental 
or other disturbance. 

Oyer calls attention to the FlG - 262 

fact that a third lower molar in 
its attempt to erupt, frequently 
causes a cellulitis, extending into 
the temporomandibular joint, 
causing acute ankylosis. 1 

Judging from postmortem re- 
cords and recent skiagraphy, 
cases of impacted third molars 
are more common than generally 
believed. Instead of remaining 
in the alveolar portion of the 
bone, the impacted tooth may 
come to occupy a cavity in some 
portion of the body or the ramus 
of the bone (Figs. 261 to 264). 
The positions of the teeth in 
such cases tend to confirm 
Tomes' theory of the develop- 
ment of the jaw. The jaw being lengthened, and the ramus develop- 
ing through conjoined deposition and resorption of bone, the crown 
of the tooth appears to be either fixed in a bony nucleus and trans- 
ported to some distant point in the developmental progress of the 
jaw, or to be irregularly shifted about during jaw growth. At later 



Wisdom tooth buried in the ramus. 
(Tomes, after Marshall.) 



Dental Cosmos, October, 1911. 



288 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

periods, the pressure exercised by root formation disturbs the rela- 
tions of the tooth with its earlier surroundings. These efforts at 
eruption may, at late periods, cause the appearance of the tooth in 
odd situations. In the case shown in Fig. 263 the crown of the 
tooth made its way through the angle of the bone and through the 
muscles and skin. The opening in the skin healed upon extraction 
of the tooth. 

Impacted Upper Third Molars. — Some phases of impaction of this 
tooth have been spoken of under the head of Pathological Dentition. 
The most common is imprisonment of the tooth and its subsequent 
partial eruption in a horizontal position, the crown pointing toward 
the cheek (Fig. 173). The crown of this tooth may, in rare cases, be 
directed inward or backward, in the latter case being arrested by 
the pterygoid plates of the sphenoid bone. It may present with 
an anterobuccal facing of the crown, as shown in Fig. 264, or with 
a posterobuccal facing. 

Fig. 263 




From a wax model in the museum of the London Odontological Society. (Tomes.) 

In a case recorded by Tomes (Fig. 265) the extraction of the 
second molar revealed the third molar in a reversed position, its 
roots occupying the depression between the roots of the second 
molar. A case has been reported, of an upper molar with the roots 
partly embedded in the floor of the antrum, its neck carious, 1 and 
the antrum in a state of suppuration. 

Impacted Cuspids. — In point of frequency of impaction the upper 
cuspids stand next to the lower third molars. The upper cuspids lie 
high up ; the floors of their crypts, in which they lie loosely, are at a 
higher level than those of the adjoining teeth; their crowns, as with 
the other anterior teeth, lie lingual to the roots of their predecessors. 
All of these are elements which might cause displacement of the 
developing cuspids. Should the advance of eruption not keep pace 
with the development of the alveolar bone, imprisonment is likely; 



Possibly resorbed or decalcified instead of carious. (Editor.) 



IMPACTION OF TEETH 



289 



again, the dense bone immediately about the first bicuspid and 
lateral incisor may offer a deflecting resistance. Examining the 

texture of the bone about these 
FlG - 2,w parts, it is evident that the 

direction of least resistance to 
the advance or a much deflected 
crown is into the cancellated 

Fig. 265 




Upper jaw, with the third molar directed 
forward and impinging upon the second 
molar. The small tooth situated high up 
in the anterior part of the jaw was forced 
there by the spade of the grave-digger. 
The artist's accuracy in delineating all 
parts of the specimen has rendered this 
explanation necessary. (Tomes.) 




A second molar of the upper jaw, 
with the wisdom tooth inverted and 
embraced within the roots. (Tomes.) 



bone of the incisor portion of the alveolar process; hence it is most 
usual to find the crowns of these teeth lying with their cusps 
pointing forward (Fig. 266). Several recorded cases have the posi- 



Fig. 266 




Abnormal jaw, showing impacted cuspids. (Cryer.) 



tions shown ; one or both of the teeth may be impacted. Cuspid teeth 
may erupt into the nasal cavity or appear in the canine fossa, and pre- 
19 v 



290 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

sent the crowns cheekwise, or lie horizontally and above the roots of 
the bicuspids. 

Fig. 267 




Impacted bicuspid. (Salter.) 

Glas, of Vienna, discovered a cuspid in the nasal floor associated 
with calcic formations in its ulcerated surface (rhinolith). The 
patient, aged nineteen years, had frequent fetid eructations, with 
vomiting of green, foul-smelling masses. With the removal of the 
cuspid the vomiting, etc., ceased. 

Fig. 268 




Lower maxilla, in which the right second bicuspid is placed obliquely, the root being 
directed backward. The crown, though exposed, does not rise above the level of the 
alveolar margirj. (Tomes.) 



Impaction of Other Teeth. — While impactions are most common in 
connection with the teeth named, any other teeth of a denture may 



IMPACTION OF TEETH 



291 



be imprisoned. Fig. 267 shows an impacted bicuspid whose root 
development has been normal as regards its length, but whose curve 



Fig. 209 




Imprisoned central incisor. (Kirk and Cryer.) 

has been modified by the resistance of surrounding tissues. Fig. 269 
exhibits an imprisoned central incisor, whose retention was, no 
doubt, determined and malposition caused by the development and 
presence of the brood of supernumerary teeth which surrounded its 
crown. 

Fig. 270 




Maxilla, in which the temporary cuspids (the sockets of which are shown by the 
dotted lines) were retained, and the permanent canines developed within the substance 
of the jaw. The bone has been removed on the one side to show the direction taken 
by the tooth, which has been twisted on its axis to the extent of a quarter of a turn. 
(Tomes.) 



Upper incisor teeth have been seen inverted and their crowns 
erupted into the nasal cavity, where they have produced inflammation, 



292 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

which later became infective. 1 A supernumerary tooth has been 
found in the floor of the nasal cavity 2 so that presence of all normal 
teeth should not exclude extra teeth from consideration in making 
a diagnosis. Skiagraphy may demonstrate an unsuspected super- 
numerary. 

Impacted teeth do not necessarily produce such pathological con- 
ditions as produce untoward symptoms. The malposition of the 
impacted teeth either in total or partial impaction may, however, 
lead to malposition of other teeth, or results 
FlG - 271 such as caries. The relation of impacted 

C* rx teeth and any ulterior disease condition is 

<\ r\ \ ^ settled by the facts, the probabilities of 
i\ r 1 ^ 1 relation, or the results of their removal. 
/ \ / A / \ Symptoms. — The most common symptom 

ps / I V J attendant upon impaction of teeth, judging 

from the obtainable records of cases, is tri- 
by ImP smiioar et opemW [ acial neuralgia of any degree, caused by 
(Cryer.) impingement of the malposed tooth upon 

nerve filaments or trunks. Cryer 3 records a 
case where a supramaxillary neuralgia was traced to the presence of a 
central and lateral incisor, and a cuspid tooth in the anterior wall 
of the antrum; they were only discovered by an exploratory opera- 
tion. A cure of the neuralgia was effected by their removal. 

Impacted third molars frequently give rise to heavy rheumatic 
pains about the side of the face and jaws, and no doubt in such cases 
as depicted in Fig. 256 would cause intractable and diffuse maxillary 
neuralgia. Salter 4 records a case of long standing and intractable 
neuralgia, exhibiting a constant painful area upon the scalp, and in 
which heat and tenderness were noticed over a swelling upon the 
hard palate. Immediate and permanent cessation of the neuralgia 
followed removal of the teeth. 

Dr. N. T. Shields 5 describes a case of great pain in the region of 
the mental foramen, accompanied by a later appearance of fever, 
reaching 103.8°, with subsequent enlargement of the submaxillary 
gland, as cured by the surgical removal of the two impacted bicuspids 
and deciduous tooth shown in Fig. 272. 

Symptoms of maxillary periostitis — heavy, gnawing, and dull, 
throbbing pain, with more or less heat and engorgement of tissues — 
are noted as an accompaniment of impacted teeth. Such symptoms 

1 Jameson: International Dental Journal, 1899. 

2 Boral: See Cosmos, December, 1911. 

3 Dental Cosmos, 1896. 

4 Dental Pathology and Surgery. 

5 Dental Cosmos, 1908. 



IMPACTION OF TEETH 293 

may herald the appearance of the tip of the tooth through its bony 
covering and gum. 

Cases of maxillary abscess, in the absence of their usual cause 
(gangrenous pulp), may run a prolonged and painful course, 1 involv- 
ing neighboring structures, which may be vital, and after free venting 
be found to have arisen about an impacted tooth. The probable 

Fig. 272 




Skiagraph showing impacted teeth. (Shields.) 

explanation for many cases is the partial absorption of the overlying 
tissues, permitting ingress of bacteria, but in some cases crown 
resorption may cause irritation, and bacteria in the blood may 
localize. A few cases of pulp exposure have been seen when a sinus 
allowed ingress of bacteria and the production of caries. In such 

1 See Garretson's Oral Surgery and Salter's Dental Pathology. 



294 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

case a pulp may die, undergo putresence, and cause apical abscess 
with its symptoms. 

Occasionally a circumscribed swelling is noted upon some aspect 
of a jaw, most frequently upon the palatal portion of the superior 
maxilla, which is attended by inflammatory symptoms, and an 
incision reveals an impacted tooth. If a plate has been worn, the 
tissue between, and even the bone may become necrotic. 



Fig. 273 



Fig. 274 



L~^ 



X-ray photograph, showing mal- 
posed cuspid entirely embedded in the 
bone and pressing upon the central. 




Impacted cuspid revealed by resorption 
of the overlying tissues. (Burchard.) 



Quickly forming cysts of the jaw, upon receiving surgical treat- 
ment, may be found to contain the crown of an entire tooth, this 
evidently being the centre of irritation from which the cystic forma- 
tion had its origin. Melancholia, mania, and dementia precox have 
been relieved by the extraction of impacted teeth diagnosticated 
by skiagraphy. 1 This shows a relation between cause and effect 
(Figs. 275, 276, 277). M. C. Smith 2 reports a case of lifelong 
attacks of prostrating sick headache due to impaction of a third 
lower molar and relieved by its extraction. 

The pulps of other teeth have been devitalized by the strangula- 
tion due to the pressure of the crown of the impacted tooth upon 
the apical tissue, and the production of pulp nodules in other 
teeth through a reflex hyperemia has been noted. The resorption 
of roots of other teeth has been produced by the pressure of the 
impacted tooth. 

Hypercementosis and concrescence have also been produced by 
the descent of the tooth and have produced impaction. 



1 Upson: Dental Cosmos, 1910, p. 527. 

2 Dental Brief, 1912. 



IMPACTION OF TEETH 295 

Resorption of the roots of the impacted teeth, or resorption of the 
enamel and dentin of the crown may occur. In one case, a calculus 
in nowise associated with the oral cavity, and divided from it by an 
area of pericemental tissue was found. (See Resorption of Enamel, 
for illustration.) 

In all these cases diagnostic features exist, though none are com- 
parable to the .r-rays. 

Diagnosis. — The first point of observance in cases of suspected 
tooth impaction or of obscure supernumerary teeth is an examina- 
tion of the dental arches. Are all of the permanent teeth in position? 
Given the absence of, for example, a lower third molar from the 
dental arch, with a history of no eruption, and a persistent neural- 
gia, particularly if occasionally accompanied by or alternated with 
heavy rheumatic, or what are known as bone pains, and finding no 
other evident cause of the neuralgia, an impacted tooth would be 
naturally inferred to be the source of the disturbance. Impacted 
teeth which lie horizontally, or nearly so, along the palatal vault 
frequently cause a swelling. This, taken in conjunction with the 
absence of a tooth from the dental arch, points to a diagnosis of 
impaction. 

In very many cases of impaction, diagnosis has been a mere acci- 
dent; discovery being made in the course of an exploratory surgical 
operation. In other cases dental disturbance has been simply an 
inference, until skiagraphy has determined an impacted tooth or 
some other lesion to be present. B. H. Catching 1 was the first 
to practically apply this diagnostic test in this connection. The 
left upper central incisor of a female, aged nineteen years, became 
loosened, and an exploration through its pulp chamber revealed 
a hard body occupying a position part way up the root, which had 
undergone resorption to that point. The cuspid of the left side was 
absent from the arch. A skiagraph of the parts (Fig. 273) revealed 
the missing cuspid, whose crown had impinged upon and caused 
resorption of the central incisor. 

Impacted teeth may become uncovered at some aspect late in 
life, and the condition be discovered incidentally. Cases are recorded 
where the pressure of a plate has caused the resorption of tissues 
overlying an impacted tooth, thus revealing its presence. Fig. 274 
illustrates a case where the presence of an impacted cuspid was 
revealed at the age of seventy years, through resorption of the 
alveolar bone and the gum tissue covering the tooth. 

As the smooth feel of enamel is a diagnostic feature when instru- 

1 Catching's Compend, 1896. 



296 MALFORMATIONS AND MALPOSITIONS OF THE TEETH 

mental examination is made, it is to be remembered that the enamel 
and dentin of an impacted tooth may undergo a true resorption 
with the characteristic Howship's lacunae. When partly exposed 
to the oral fluid, caries may occur. Both these conditions produce 
rough surfaces, but enamel may usually be felt at some point. 

Fig. 275 Fig. 276 





Impacted lower third molar; cause of Cuspid tooth, unsuspected by patient ; 

neuralgia. (Skiagraph by Lodge.) demonstrated to have been responsible 

, for severe neuralgias. Patient, a 

draughtsman, had not been able to 
work at his business for the six months 
previous. The tooth was not known 
to be present, until revealed by x-rays. 
It was removed from the lingual side. 
(Skiagraph by Lodge.) 

Fig. 277 




Impaction of upper third molar, without local pain, cause of profound delusions and 

melancholia. (Upson. 1 ) 

Treatment. — The treatment of cases of impaction is the removal of 
the offending tooth. Whether or not this comes within the province 
of the dental operator depends upon the position of the tooth, and, 
incidentally, upon the usual range of practice of that particular 
practitioner. When the tooth is embedded deeply in the substance 
of the jaw, access to it involves the anesthetization of the patient, 

1 Insanity Caused by Painless Dental Disease, Dental Cosmos, 1910. 



IMPACTION OF TEETH 297 

and the removal of the bone which obstructs the path of extraction; 
this may be an operation of some magnitude, and is usually done by 
a special surgical practitioner. When, however, it is evident that 
the obstructions to the removal of the tooth consist of the soft 
tissues and but a lamina of bone, the operation for removal is clearly 
within the province of the dental operator. For example, the pres- 
ence of an impacted cuspid is determined, lying horizontally along 
the lateral aspect of the roof of the mouth. The parts may be 
injected with a local anesthetic solution, and a cut made with a 
sharp bistoury through the soft tissues from the outside of the 
swelling, to the bone. The flap thus outlined is raised from the 
bone, the flap including the periosteum. A large, sharp bur is then 
employed to remove the covering bone. When the tooth is freely 
exposed it may be dislodged with forceps or elevator. The parts 
are then washed with a hydrogen-dioxid solution, dried, the flap 
pressed back into place, and steresol 1 painted over the parts, or 
a stitch or two may be taken before application of the steresol. 
The mouth should of course be kept as aseptic as possible both before 
and after operation. A simple clot kept aseptic may be sufficient. 

1$ — Purified gum lac gix 

Purified gum benzoin 5 f 

Balsam of tolu 5 i 

Oil of cinnamon (Chinese) S^ 

Carbolic acid giij 

Saccharin o} 

Alcohol Oij — M. 

1 Dental Cosmos, 1S95. 



SECTION III. 

AFFECTIONS OF THE ENAMEL AND DENTIN. 



CHAPTER IX. 
ABRASION, EROSION, AND MECHANICAL INJURY. 

Formed by the ameloblasts, which are later changed into Nasmyth's 
membrane, and borne upward with the crown during the process 
of eruption, enamel has no posteruptive source of nutritive supply 
from without. 

Its only conjectural source of nutrition is, therefore, from the 
pulp via the dentinal tubuli. This seems to have been proved by 
Caush, and later by others. (See p. 173.) Teeth do change in color 
with advancing age, generally becoming yellower; this is probably 
due to tubular calcification (which see), rendered possible by the 
tubes containing organic matter which are now supposed to permit 
a slow interchange of nutritive sap. 1 This coloration may be seen 
in cases of abrasion and in some cases extends even into the second- 
ary dentin associated. The editor has a patient with a vital tooth 
of mahogany brown color, which she claims changes the depth of 
color. Changes in the color of the dentin may be transmitted 
through enamel, which is normally almost or even quite transparent. 
Such a transparency may be seen at the incisal edges of thin incisors 
before these edges are worn down. Another proof of transmission 
of color through enamel is seen in caries; a bluish-black or white 
appearance is caused by the decayed mass or decalcified inner surface 
of the enamel. 

Again, amalgam or gold, oxyphosphate or oxychlorid, reflects its 
color through enamel, and, in excavating, the shadow of the excavator 
may be seen through thin walls. Enamel may be stained or whitened 
by decalcification due to causes acting externally. Extreme polishing 

v l C. Francis Boedecker: Dental Cosmos, September, 1911. 

(299) 



300 AFFECTIONS OF THE ENAMEL AND DENTIN 

may also cause a new character of light reflection, simulating a change 
in color. Talbot claims a change in color of teeth during prolonged 
illness, such as pneumonia, typhoid fever, syphilis, tuberculosis, and 
in pregnancy. 1 With advancing age, the translucency of teeth 
verges more toward transparency — apparently a sclerotic change 
in the dentin. (See Transparency.) 

After implantation, a tooth may somewhat change its color, but 
this evidently cannot be due to nutrition from the pulp, as this 
organ will have been removed before implantation. It would seem 
that it may take up coloring matter from the saliva. 

Enamel may suffer mechanical and chemical injury, but whether 
it may undergo constructive changes or retrograde metamorphosis 
is at present only conjectural. There is, however, a possibility 
that a molecular change may occur as a result of slow interchange 
of fluid, environment, or impact of mastication. 

The dentin and cementum contain about 28 and 30 per cent, of 
organic matter, respectively, and stain deeply and permanently with 
great readiness. 

Possessed of living cells, they also undergo changes in their structure 
under the influence of various stimuli, their substance being added 
to or reduced according to circumstances. They are also acted upon 
by mechanical and chemical agencies, if exposed to their influence. 

ABRASION. 

Abrasion is the mechanical wearing away of tooth substance. 

Occurrence. — It occurs most commonly upon the occlusal surfaces 
of teeth, but is also found upon the approximal and labial surfaces, 
the labial cervix, and more rarely upon the lingual surfaces. It is 
also seen in the temporary denture, especially in the molars, and 
is found in animals (Figs. 288 and 289). 

Appearance. — Purely abraded surfaces present a smooth, flat, or 
concaved, highly polished appearance. The surface may become 
stained or otherwise altered in color, or subsequent caries may 
remove its smooth surface. 

Occlusal Abrasion. — Occlusal wear is very common, and occurs 
largely with men who chew tobacco; the contained silex, being gritty, 
acts as an abrasive. Such wear, due to the use of hard food or gritty 
substances, is seen in skulls of aboriginal man. Ottofy describes a 
peculiar form of wasting due to chewing betel nut mixed with bay 
leaves and slaked lime. No doubt a gritty element is introduced. 

1 Dental Cosmos, 1905, p. 29. 



ABRASION 301 

Some degree of occlusal wear is accepted as normal to all teeth, the 
act of mastication producing marks or facets at the point of articu- 
lation of antagonizing teeth. A tip-to-tip variety of occlusion 
permits free lateral movement of the lower jaw, and a herbivorous 
type of articulation causing abrasion. It is also frequent in those 
cases presenting the first degree of prognathism. In some of these 
cases, the labial surfaces of the upper incisors and cuspids, and the 
linguo-incisal margins of the lower incisors are worn. A single over- 
lapped lower tooth may abrade an upper tooth in this manner. 

The gritting of teeth is also a cause. This gritting, termed f bruxo- 
mania,f may occur only at night or for a few minutes each day; 
again it may appear for entire days, weeks, and months, not ceasing 
even during sleep. In such cases the teeth are worn down flat. 
Maria and Pietkiewicz 1 noted 12 cases of central nervous lesions, 
mostly dementia, developing bruxomania; also it has been noted in 
cases of epilepsy and chorea. 

A clay pipestem may wear a hole of its own diameter in the incisal 
edges of anterior teeth; other stems wear less. Upholsterers and 
seamstresses have peculiar abrasions (tack holding, thread biting). 

Fig. 278 



Abrasion of anterior teeth, with loss of posterior occlusion. (W. A. Capon.) 

The undue loss of posterior occlusion and consequent overuse of 
the anterior teeth cause their abrasion after the manner show r n in 
Fig. 278. A marked overbite, produced in any manner, may cause 
lingual abrasion of upper anterior teeth. 

Where the abrasion occurs in a fairly regular manner, four degrees 
of abrasion are classified: (1) Abrasion removing the cusps; (2) 
abrasion removing the occlusal third of the crown; (3) abrasion 
removing the middle third of the crown; (4) abrasion extending to 
the gum line or beyond. (Broca.) (See Figs. 279 and 280.) 

When there is a marked overbite occlusion, with a consequent 
lessening of the lateral movement of the mandible, the teeth do 

1 Dental Cosmos, 1907, p. 525. 



302 



AFFECTIONS OF THE ENAMEL AND DENTIN 



not acquire flattened contact surfaces, but their cusps increase in 
sharpness and pointedness. This at times becomes exaggerated, and 
produces an interlocking of cusps or rather worn surfaces which 
have very sharp edges. 



Fig. 279 




The first and second degrees of abrasion. Specimens from museum of Philadelphia 

Dental College. 



Fig. 280 




The third and fourth degrees of abrasion. Secondary dentin plainly visible. Specimens 
from museum of Philadelphia Dental College. 



In the first degree of abrasion, the dentin is often hollowed out in 
advance of the enamel of the cusps, forming concave places in which 



ABRASION 303 

berry seeds lodge and cause annoyance. These spots are at times 
hypersensitive. The plane surfaces also are often sensitive upon 
merely rubbing the teeth together. 

Labial and Approximal Abrasions. — Some forms of abrasion have 
been attributed to too vigorous use of tooth-brushes, particularly 
when gritty powders are employed. There is no doubt that mechan- 
ical abrasion about the necks of teeth is produced in this manner, the 
gum line receding beyond the enamel border, exposing the cementum; 
and a careful examination will reveal the cementum and next the 
underlying dentin to be affected; the enamel, when abraded, shows 
first as a facet, then as a spot of bare dentin with thin edges of enamel 
around it (see the left lateral in Fig. 299), and later the area may be 
grooved. As a rule, however, the effect shown in Fig. 298, lower 
jaw, is the more common. These tooth-brush abrasions are quite 

Tic. 2S1 




Abrasion due to employment for twenty years of a gritty English tooth paste. 
At 7, gold crown abraded. (Miller.) 



characteristic. In well-kept dentures, the gums are seen to have 
receded from their normal line, but may exhibit little evidences of 
turgescence; the roots of the teeth, upper and lower, are exposed to 
a greater or less extent along their labial and buccal, but not usually 
along their lingual aspects; and they are excavated to variable 
depths, upon the bicuspids and first molars more than upon the 
other teeth, as here the greatest force of brushing is received. The 
depressions have a normal dentin color, sometimes deepened in the 
mouths of non-smokers, and which in smokers may be periodically 
blackened by deposits of carbon. If caries supervene, the abraded 
areas lose their normal color, and may be readily indented by sharp 
instruments, which they resist before the advent of caries. The 
bicuspids and molars, particularly, may be grooved in such manner 
as to require restoration by fillings. 



304 AFFECTIONS OF THE ENAMEL AND DENTIN 

Fig. 282 




Photomicrograph of sediment obtained by washing tooth paste, which caused the 
abrasion shown in Fig. 281. (Miller.) 



Fig. 283 



A B c 




Abrasion of lingual surface by assiduous brushing with tooth powder. At D and E 
amalgam worn down. (Miller.) 



ABRASION 



305 



Miller 1 investigated this subject very carefully, and found that 
the grit in many forms of tooth powder, vigorously used, was quite 



Fig. 284 




Artificial abrasion produced by brushing with a much-used English tooth paste with 
motor brush for eighteen hours. Remains of gold filling in first bicuspid. (Miller.) 

Fig. 235 




Gradual wear of both tooth substance and filling material, notwithstanding the open 

bite. (Miller.) 



competent to wear away tooth structure, gold, and other fillings 
(Figs. 281 to 284). Figs. 283 and 286 show a lingual wasting, 

1 Dental Cosmos, 1907. 
20 



306 AFFECTIONS OF THE ENAMEL AND DENTIN 

resembling graphic erosion. In both cases abrasion is proved by 
the wasting of metal, which acids could hardly accomplish. Miller 
experimentally proved abrasion competent to produce the grooves 
known as "wedge-shaped defect" (Figs. 284 and 298). 

Calculus may be worn in like manner, either by the brush or by 
the festoon of a plate (Fig. 287). 

Miller found that among clinic patients who never used a tooth- 
brush the labial abrasion was wanting, and he observed that a 
cessation of wear followed the abandonment of the use of gritty 
powder and the adoption of a soft brush and mild powder, which is 
the evident indication in such a case. 

A clasp may abrade a tooth, and, if food debris be retained on its 
inner side, caries may follow in the abraded area. The purely abraded 
surface will be polished. Slight approximal abrasion may be normal 
as a facet, due to the rubbing of one tooth upon another at the 
contact point. A marked example of this was seen in the mandible 
of a skull of a Maori. (Museum of Philadelphia Dental College.) 

The third lower molars are locked beneath the distal surface of 
the crowns of the second molars. Some form of bone loss occurred, 
producing looseness of the third molars. The individual motion of 
the teeth produced a deep abrasion of the enamel of the second 
molars upon the distal surface, and an occlusoproximal abrasion of 
the third molars. (Also see Fig. 338.) 

Grit in powder may easily be detected by taking a small portion 
between the incisor teeth, or may be found by elutriating the 
powder, i. e., place in water, stir, let settle for a few seconds, pour 
off the supernatant fluid, and examine the sediment as above, Or 
microscopically (Fig. 282). 

Miller found from experiments, as to the effects of various acids 
acting for a time and followed by brushing with abrasives, that it 
depends very materially upon the nature of the acid. Those acids 
which rapidly decalcify (soften) the dentin, of which we may take 
hydrochloric and lactic as types, most readily retard the wearing 
away by friction (unless the friction be so great as to wear in spite 
of the decalcification). While those which act slowly on the dentin 
(oxalic, tartaric, etc.), as well as those which have a macerating 
effect on decalcified dentin, may be wanting in this influence. He 
concluded that wear could not be produced by acid alone, but that 
any acid or acid salt which possesses the power of extracting the 
calcium salts from enamel, or of breaking up the connection between 
the enamel prisms, may accelerate the process of wasting, provided 
the necessary mechanical factor works together with it. Miller 
found food to be a negligible quantity as to wear upon labial surfaces. 



ABRASION 307 

The editor has a patient presenting the general characteristics of 
Pig. 300, who has been a brush enthusiast, and was taught in early 
life to use a toilet soap containing fine pumice (Bazin's poncine soap). 

Extensive approximal abrasion may be due to extrusive elonga- 
tion of a tooth in one or both jaws, causing a tooth to occlude with 
its antagonist with a glancing motion. 

In this manner, specimens are produced abraded from the occluso- 
approximal angle to nearly the apex of the root. 

The festoon of a metal plate may rapidly cause abrasion of the 
lingual cervix of a tooth. The condition is, however, rare; caries 
being more common. In the editor's practice a case was seen, in 
which several teeth were so affected in a few months, by an ill-fitting 
metal plate. The festoon of a vulcanite plate has also produced 
such an abrasion. 

Abrasion sometimes follows caries, when the latter has become 
freely exposed to attrition. The softened surface wears away and 
the part assumes a polished appearance, but is discolored as the 
result of the stain due to the caries. (There is also eburnation, 
which see.) 

It is probable that a hyperacid condition of the saliva in con- 
nection with mechanical forces may be a cause of rapid abrasion. 
(See Erosion.) 

Effects of Abrasion. — These are external and internal, and most 
marked in the occlusal variety. The crown wears down until at times 
the gum is reached. In the process sharp edges of enamel are formed. 
These splinter off, leaving rough edges, or the enamel may fracture 
or split longitudinally, following the axis of the crown. Supported 
by dentin it does not further break away (Fig. 308). 

Sharp enamel edges may irritate the tongue, producing ulcers of a 
sometimes chronic type, which acquire indurated edges and simu- 
late syphilitic sores or epithelioma. The causal relationship between 
sharp edges of the teeth and lingual epithelioma appears to be quite 
clear in some cases. Brown 1 mentions a case of tetanic spasms of 
masticatory muscles due to this source. 

Sores which have given evidence of malignancy and been diagnos- 
ticated as malignant growths, have been cured by rounding and 
polishing sharp and irritating enamel edges of teeth. 

The continued stimulation of the ends of the dentinal fibrillar, which 
are exposed in abrasion, causes them either to become hypersensitive 
or stimulates them to formative activity. Tubule material is built 
upon the inner walls of the tubule, obliterating their lumen. This 

1 Dental Cosmos, 1908, p. 4. 



308 AFFECTIONS OF THE ENAMEL AND DENTIN 

Fig. 286 Fig. 287 




a, abrasion of lingual surfaces; b, of 
amalgam filling produced by a plate. 
(Miller.) 




Abrasion of calculus. (Miller.) 



Fig. 288 



Fig. 289 




Abrasion of lower incisors of a horse Defects resembling wasting in the teeth 
produced by "cribbing." (Miller, after of a sea lion. (Miller, after Murie.) 

Kitt.) 



ABRASION 309 

is the so-called tubular consolidation or calcification (eburnation). 
Accompanying this, secondary dentin is often formed. As a result, 
most commonly the pulp chamber of the crown is filled up with 
secondary dentin as the abrasion proceeds, and the crown may often 
be worn off until the cervix is reached, while the pulp remains vital 
and covered (Fig. 280). In some cases the abrasion closely ap- 
proaches the pulp, which has failed to protect itself, probably because 
of atrophy of odontoblasts, and the phenomena of hyperemia, or 
even exposure, and its results occur. A left upper bicuspid of the 
second skull in Fig. 280 was in this state. 

The causes and phenomena of abrasion of the temporary teeth are 
practically the same as in the case of adults, except, perhaps, that 
children are more subject to the action of rectal parasites, as ascaris 
lumbricoides, tenia, etc., or suffer from irritable bladder due to 
hyperacidity of the urine. These conditions commonly produce a 
reflex stimulation of the muscles of mastication, resulting in nocturnal 
gritting of the teeth. 

Fig. 290 




Same case as Fig. 278. Bite opened by bridge-work, posteriorly. Anterior teeth 
restored by means of Land jacket crowns. (W. A. Capon.) 

Treatment of Abrasion. — In the cases of cupped occlusal dentin, 
hard fillings of platinum gold or platinized, gold inlays are best. 
Whether the filling be built in or an inlay be set, it is advisable not 
to cut too closely to the enamel in making the cavity, for the struc- 
ture of such a wall is often fractured after filling when this is done. 
If possible the form in Fig. 291, with retention made elsewhere than 
near the side enamel is preferable. Inlays requiring only pin 
anchorage are preferable when undercutting would weaken. 

If nearly all teeth are present and the abrasion slight, bridge-work 
may be used to restore the full occlusion without attempt at restora- 
tion of the worn surfaces. 

If the abrasion of the upper anterior teeth be deep, the bite may 
be raised by appropriate posterior crowns or bridges, and solid 
platinum-gold fillings may be built upon the anterior teeth, either 



310 



AFFECTIONS OF THE ENAMEL AND DENTIN 



Fig. 291 



the uppers alone or upon both the upper and lower teeth. Anchor- 
age may be obtained in the dentin, or screws may be planted in the 
dentin between the enamel and pulp and the fillings be built about 
them. Instead of malleted fillings, tips of the gold-inlay type may 

be made (Figs. 292 and 293). Casting the 
inlay is a simpler method. Usually it is 
better to use an alloy of iridioplatinum 
gold. This applies also to the lingual 
occlusal abrasion of incisors. 

For those cases in the second degree, 
as a means of limiting the abrasion, Dr. 
J. C. Curry has introduced small trun- 
cated cones of unannealed iridioplatinum, 
which are to be cemented into holes 
drilled into the occlusal faces of the molars 
and bicuspids with an inlay drill of exactly corresponding size, 
mounted in the right-angle hand piece. As many are put in as 
the safety of the pulp and the enamel will permit. They act upon 
the same principle as steel nails in a shoe heel. 




Manner of preparing the 
outer retaining wall of a 
cavity in case of cupped oc- 
clusal abrasion. 



Fig. 292 



Fig. 293 



Fig. 294 







Gold tip for abraded 
teeth with living pulps. 
(Evans.) If cast the mar- 
gins are to be beveled out- 
wardly. 



Gold tip for abraded 
teeth with pulps re- 
moved. (Evans.) 



Porcelain-faced crowns 
for teeth with living pulps. 
(Evans.) 



In other cases, after securing a proper opening of the bite and 
posterior occlusion with crowns or bridges, single porcelain-faced 
gold or platinum crowns may be made to cover each of the anterior 
teeth. For this purpose the crown is appropriately reduced to 
convenient form, but the t pulps need not be destroyed. Fig. 294 
represents the method outlined by Evans. 1 There can be no objec- 
tion to pulp removal in any of these cases, if for any reason a dowelled 
crown seem preferable. 

1 Crown and Bridge Work. 



ABRASION 311 

Land jacket crowns, consisting of a wedge-shaped platinum jacket, 
with a porcelain facing attached by means of one of the numerous 
inlay bodies, may be used instead of the Evans crown. In some cases 
other forms of crowns may be indicated (Fig. 290). 

There present at times cases of abrasion in which, aside from the 
wear, pyorrhetic conditions may be present, or where bridges cannot 
be properly inserted, especially when only a few teeth remain. 

If this pertain to the upper jaw T only, the lower denture may be 
restored to usefulness, the upper teeth extracted, and a full upper 
denture inserted; this permits the adjustment of the bite to any 
desired level. If the conservation of a few teeth is desirable, they 
may be crowned or bridged; the occlusion being raised if desirable, 
then a plate constructed. If the condition be transferred to the 
lower jaw and the anterior teeth be in good condition, a piece with 
the Roach 1 or Morgan type attachment may be fixed upon cuspid 
or bicuspid crowns. 

It is to be remembered that in any case of opening of the bite, the 
occlusion is to be restored throughout. 

The bite must not be raised by means of partial plates which strike 
before the natural or crowded teeth, as they tend to embed them- 
selves in the soft tissues and create inflammation. 

If the bite be only slightly raised by plates, this embedding will 
cause a return to the original condition. Neither must too great a 
strain be placed upon supporting teeth (see Overwork of Teeth). 

In case of hypersensitivity, Robinson's remedy, silver nitrate, 
nitric acid, or the actual (hot burnisher) or the electrocautery may 
be effective; if not, the areas should be excavated and filled, or, if 
necessary, the pulp should be devitalized. 

If the abrasion be caused by tobacco its use should be stopped. 

A difficult class of cases to treat is found in those highly nervous 
individuals who grit their teeth during sleep. It is probable and 
reasonable that this cause alone may serve to explain abrasions trace- 
able to no other source. The cure of such cases as these could only 
be possible through the wearing at night of some modified form of 
interdental splint. Arnone has described a simple vulcanite splint 
for the low T er teeth, to open the molars about one-sixteenth of an 
inch and the incisors one-half inch. This he calls "the insulator," 
and is to be vulcanized at 160° C. It is to have the upper surface 
rounded (Fig. 295). He also describes "the paraglossus," a double 
vulcanite splint made in one piece to be inserted by bruxomaniacs 
during sleep, or by epileptics during the forewarning "aura," if 

i Dental Cosmos, 1908, p. 17. 



312 



AFFECTIONS OF THE ENAMEL AND DENTIN 



present, to prevent grinding or tongue biting. 1 The cases naturally 
indicate the medicinal use of a bromide before retiring, unless the 
causes can be discovered and removed. 

If such gritting be present in children, the evidences of irritable 
bladder, due to hyperacidity of the urine, or of rectal parasites, should 
be sought and treated. The urine may be rendered alkaline by the 
use of potassium salts, and kept so by restriction to a largely vegetable 
diet. Belladonna may be used to reduce vesical irritability. Rectal 
parasites may be removed by the use of vermifuges, or, occasionally, 
by rectal injections. 



Fig. 295 



Fig. 296 





The "insulator." (Arnone.) 



The " paraglossia. " The meta 
groove shown relates to another 
method of construction. 



Fig. 297 



RESORPTION OF ENAMEL. 

Definition. — Resorption of enamel is the removal of enamel sub- 
stance by soft tissue containing osteoclasts. 

Occurrence. — It occurs externally only 
in impacted teeth surrounded, at least 
in part, by irritated tissue, and internally 
very rarely after resorption of dentin by 
the pulp 2 (Fig. 297). (See Pulpitis.) 

Such tissue may also be found in der- 
moid cysts, and causes the resorption of 
teeth. (See Fig. 32.) 

Pathology and Morbid Anatomy. — Osteo- 
clasts approximate the enamel as they do 
cementum, decalcify and resorb it. The 
There result irregular excavations (How- 
ship's lacunas) and white or discolored areas of evident slight decal- 
cification of the enamel. A deposition of bone into the area may 

1 Dental Cosmos, 1908, p. 924. 

2 Hopewell-Smith: Histology and Pathohistology of the Teeth. 




Impacted cuspid with re- 
sorption of enamel and a 
hematogenic calculus. 
(Miller.) 

dentin is next attacked. 



EROSION 



313 



occur. 1 The process is probably the result of a non-septic inflam- 
mation, as in the case of root resorption. (See Interstitial Gingivitis 
and Resorption.) 

The enamel may be resorbed from its internal surface after the 
resorption of dentin by the pulp (see Chapter XVI), and, as shown 
by Woods, may be filled in with adventitious material of a structure 
resembling cementum. 

Treatment. — Should the disease by chance occur upon a tooth 
which later has been drawn into place, the area may be filled; 
otherwise it has only a pathological interest. 



Fig. 298 



Fig. 299 




Case described as erosion. (Darby.) Case described as erosion. (Darby.) 

Fig. 300 





A case of erosion (drawn from the cast) : B, silhouette from a perpendicular line through 
the left centrals, upper and lower, showing the loss of substance. (Black.) 



EROSION. 

Definition. — Erosion of the teeth is a term applied to the chemical 
or chemicomechanical destruction of the hard tissues of the teeth 
in such a manner that broad, shallow, smooth excavations are 
made in the enamel and dentin in situations free from attrition 
by mastication. 

1 Hopewell-Smith: Histology and Pathohistology of the Teeth. 



314 AFFECTIONS OF THE ENAMEL AND DENTIN 

Figs. 298, 299, and 300 illustrate the characteristic appearance of 
areas until recently supposed to be due to the chemical or chemico- 
mechanical solution which has been termed erosion. 

The demonstrations of Miller with reference to abrasion of labial 
and lingual surfaces of teeth by means of the tooth-brush and gritty 
powders, and the abrasion of approximal surfaces into grooves in 
animals by the drawing of gritty grasses, etc., through or along the 
teeth, or the gnawing of bones by carnivora, etc., have cast a heavy 
cloud of doubt upon the chemical etiology of what have been usually 
considered as erosions due to the action of acid sodium phosphate 
excreted by the mucous glands of the lips or cheek. 

The appearance illustrated in Fig. 298, lower jaw, and in Figs. 
299 and 300 might readily, in the light of Miller's demonstrations, 
be regarded as abrasion, if the causes (brush and abrasive powders) 
he suggests be found; but the graphic outlines shown in Fig. 298, 
upper anterior teeth, seem difficult to harmonize with the abrasion 
theory. The cases of this sort are rare as compared with the others, 
the editor recalling but two having the peculiar undercut mesial and 
distal erosion borders. The spreading of brush bristles, as the brush 
is brought from the gum down, might account in part for this, but 
in one of the cases mentioned there was also an undercut at the 
incisal border, which would render the theory difficult of application. 

One case was in a man aged forty-five years, a German Jew, 
fond of wines, beer, etc., at meals; the other a middle-aged maiden 
lady of nervous temperament, with whitening hair, slightly wrinkled 
skin, and some evidences of goutiness. 

According to Miller, acids or acid salts, which can extract calcium 
salts, may accelerate the wasting process provided the necessary 
mechanical factor works with it and wears off the decalcified tissue 
before it becomes leathery, when wear is retarded. Kirk burnt 
asbestos cloth, treated it with hydrochloric acid, neutralized this 
with ammonia, washed it with distilled water, and again subjected it 
to high muffle heat. This absorbent, inorganic cloth he applied to 
buccal glands for twenty or thirty minutes in cases of erosion, dis- 
solved the mucus obtained in distilled water, dialyzed the salts out, 
and examined the evaporated residue under the microscope and by 
reagents. He found acid sodium phosphate to be the decalcifying 
agent in what he called graphic (hydroglyphic) erosions (Figs. 298 
and 299). 

Head 1 found by experiment with a 1 to 20,000 solution of acid 
sodium phosphate in water, acting in the incubator at body temper- 

1 Dental Cosmos, 1907. 



EROSION 315 

ature, that superficial decalcification of enamel occurred after four- 
teen hours, and when polished off it again decalcified in eight hours, 
and was quite superficially decalcified in two days; that a 5 per cent., 
2 per cent., 1 per cent., and 1 to 500 solution acted under similar 
conditions in seventeen hours, and points out that a solution of 1 
to 10,000 and 1 to 20,000 acid sodium phosphate in alkaline saliva 
acted after eight and five days only. He also has shown that enamel 
which was experimentally slightly decalcified, again hardened w r hen 
placed in saliva for a time. He was, however, unable to explain the 
result. 1 

Miller found the slowly acting acids do not produce such decalci- 
fication as to retard the abrasive action of brushing with a 10 per 
cent, pumice. Given, then, a decided production of acid sodium 
phosphate by the buccal glands in contact with the labial surfaces 
of teeth (Kirk) for eight hours (the period of sleeping, and Head's 
period of one experiment, see above), it is quite reasonable to suppose 
that an undetermined percentage of acid sodium phosphate dissolved 
in buccal mucus, which in total has an acid reaction to litmus (Tru- 
man, Kirk, and others), is competent to produce a superficial decal- 
cification, which the morning brushing will remove. This repeated 
for months or years may produce the effect seen. Brubaker, in 1894, 
immersed a tooth for a week in a solution of acid sodium phosphate, 
subjecting it daily to tooth-brush friction, and at the end of that 
time spots and grooves resembling erosion made their appearance. 

According to Head and Kirk, the acid phosphate does not attack 
the enamel so as to roughen it, but leaves it translucently smooth and 
white, and this mildness of the action of the acid sodium phosphate 
is just the action that would make smooth erosion with a minimum 
of abrasion. (See Miller's experiments, p. 306.) 

Head points out "that 1 to 500 lactic acid in water will decalcify 
enamel in thirty minutes, while the same percentage in saliva does 
not do so in fifteen days, but that the inhibitory effect of saliva is 
overcome when the lactic acid has a strength of 1 per cent." The 
inhibitory effect, therefore, seems to lie in the relative relations of 
the acid and alkaline element, though Head has shown that a mix- 
ture of 1 per cent, solution of acid sodium phosphate with a 1 per 
cent, solution of tribasic sodium phosphate, which is capable of 
turning blue litmus red, but not of turning red litmus blue, placed 
the acid under control so that the mixed solution did not corrode 
the* tooth placed in it, w r hich a 1 per cent, solution of acid sodium 
phosphate in water would do. 

1 Dental Cosmos, 1910. 



316 AFFECTIONS OF THE ENAMEL AND DENTIN 

Regarding the production of the abnormal exudate from the labial 
glands, Kirk argues that in diseases of suboxidation (resulting in 
hyperacid conditions such as gout and rheumatism) the blood is 
loaded with carbonic acid as a result of faulty metabolism. In the 
epithelium of the kidneys, the mass action of the carbonic acid upon 
the sodium phosphate of the blood, normally produces acid sodium 
phosphate, which is eliminated in the urine, and sodium bicarbonate, 
which is returned to the blood and maintains its alkalinity (see p. 96), 
according to the following reaction: HNa 2 P04+H2C03 = H 2 NaP04 
+HNaC0 3 . If the amount of carbonic acid be of only normal pro- 
duction, this action will result in only a normal amount of acid 
sodium phosphate in the urine and perspiration; but if in excess and 
not cared for by the lungs, skin, and kidneys, the buccal glands 
may also take up the action and excrete acid sodium phosphate 
'in an identically similar manner. The acid calcium phosphate is 
also found in the saliva at times, and can be formed in a similar way, 
the calcium phosphate being substituted for sodium phosphate as 
the basic salt. 

Kirk states that in the saliva of arthritics there are frequently 
found acid salts, such as acid sodium phosphate and acid calcium 
phosphate. The excessive amount of carbonic acid accounts for the 
excessive loss of phosphate in the kidneys seen in arthritics, as the 
acid sodium phosphate and acid calcium phosphate require for their 
production the basic phosphates, and the elimination of those, con- 
tinuously, produces a phosphaturia until depletion of phosphates 
occur, when their amount lessens and other salts appear. (See p. 96.) 

In a paper published in 1902, Kirk 1 describes polariscopic obser- 
vations made upon saliva from a patient afflicted with a general 
erosive wasting of the teeth. The patient had had attacks of in- 
flammatory rheumatism, and suffered from obstinate constipation, 
periodic attacks of migraine, headaches, and neuralgia, and his 
saliva was most acid at night. The saliva was dialyzed, the dialysate 
concentrated, and found to contain lactic acid salts, calcium lacto- 
phosphate, calcium lactate, and magnesium lactophosphate (Fig. 
301). 

In view of these two classes of cases, Kirk has suggested that 
erosion cases may be of two kinds: (1) A general erosion, in which 
all of the surfaces are uniformly involved, and in which lactic acid is 
the solvent agent; and (2) cases distinctly due to an exudate from 
abnormal buccal glands or gland, the acidity of which is due to either 
acid sodium phosphate or acid calcium phosphate. Talbot 2 claims 

1 Items of Interest. 'Dental Cosmos, December, 1907. 



EROSION 



317 



that the systemic acidosis produced by various diseases and by fruit 
eating in excess is responsible for the acidity of the buccal mucus 
and saliva, and for pulp and gingival degeneration and resorption 
through a process of artery and nerve-end degeneration. A decrease 
in the nprmal acidity of the urine (below 30) indicates renal insuffi- 
ciency, and the difference indicates the amount retained in the 
system. An excessive acidity of the urine indicates excessively 
imperfect oxidation. This expression of the cause is quite compatible 
with the view of Kirk, and both are views of general malnutrition. 
(See p. 93, etc.) 

Fig. 301 



1 






r» i* 




' ^i 


i0& 


fX\ 


*■* '-M>* 


if 

.... w% 


IN? 


1 : v v.^y ( . 


Br 


■ 3 S!r ■-> 




■;xh! 


wLj 




\^ ■ 




^«^R5; 




«v\ 




■ 






p* ' 




M 


m 


& " 


41 


1 ■ 




ft y 


V "H 


f 







Crystallization of salts from dialysate of saliva from erosion case, showing two typical 
forms. Large crystal is calcium lactate. (Kirk.) 



The disease appears to affect females more than males; appears 
usually after thirty years of age, and often some history of goutiness, 
arthritis, or rheumatism can be obtained. Miller denied the presence 
of this disease in the gouty, but since his observation the editor 
has had several patients hold up gouty fingers when questioned as 
to a possible gout as a cause of the erosions present. 

Erosion Due to Extraneous Acids.— Miller 1 describes a case re- 
ported by Davenport, 2 of Paris, of a healthy man whose teeth were 
eroded and worn away by acid vapors, within six months of entering 
a factory devoted to the manufacture of nitric and sulphuric acids. 
This effect was observed upon the other workmen also, and also in 
workmen in a dynamite factory in which these acids are used. The 
teeth were first set on edge. Miller suspended a tooth in a flask con- 



Dental Cosmos, 1907. 



Transactions American Dental Association, 1881. 



318 AFFECTIONS OF THE ENAMEL AND DENTIN 

taining equal parts of nitric and sulphuric acid, and found that the 
vapors attacked not only the inorganic but the organic portion as 

Fig. 302 




Another field from the same specimen as Fig. 301, also showing two typal forms 
Large crystal is calcium lactate. (Kirk.) 

Fig. 303 




Crystallization from solution of a tooth in 1 per cent, lactic acid. Large crystal is 

calcium lactate. (Kirk.) 

well, so that upon slight rubbing with a soft tooth-brush the tissue 
was worn away, leaving a hard, polished surface. Miller states that 



EROSION 319 

the vapor is nitrogen peroxid, N2O4. Lemon juice, even in lemonade, 
and vinegar will produce this effect of setting on edge, which undoubt- 
edly is due to the chemical solution of a small portion of the enamel, 
probably the interprismatic cement substance, leaving the enamel 
globules a trifle higher, this soon being worn off to a general level 
again. 

Guilford 1 mentions a case of erosion caused by shaddock (grape 
fruit) eating. Tomes cites cases of erosion caused by lemon and 
grape sucking. The pitting of grapes has produced cases of peculiar 
erosion of the labial and lingual surfaces and incisal edges of anterior 
teeth. In one case, the incisal anchorage of an approximal gold 
filling was almost worn away upon the tooth most used to pit the 
grape. Unquestionably, other fruit juices might act in a similar 
manner if the acid has an affinity for tooth structure, and the expo- 
sure to its action is sufficiently lengthy and often enough repeated 
to produce effects. 

The Effects of Erosion. — Tubular calcification and secondary dentin 
are produced together with atrophic changes in the pulp, due to 
secondary dentin formation. Gold and amalgam fillings are left as 
raised islands by the wasting of the tooth around them, though 
Miller has shown that associated abrasions may cause their wear, 
which acids evidently can hardly be expected to do. 

Scratches shown as lines and Baume's clefts are explainable upon 
the theory of abrasion by brush and powders; though usually trans- 
verse, there are sometimes vertical lines. The stimulation of the 
dentinal fibrillar by acid or mechanical stimuli may cause great hyper- 
sensitivity; as a rule, however, this is not pronounced (Fig. 304). 

The anterior teeth are sometimes shortened so that their occlusion 
is lost. Kirk's lactic acid case was of this order. The carious process 
may become implanted upon an eroded area, or at some part of it, 
usually the cervical portion. Whether this is initiated by a decal- 
cifying process due to the acid sodium phosphate, or uncleanliness 
due to a cessation in the intensity of the brushing, is not so clear as 
it formerly seemed, when it was thought due to a temporary cessation 
in production of acid sodium phosphate, which was regarded as 
immunizing the part to caries. In any event the stain of iodin is 
taken, showing the presence of bacterial films at the point showing 
caries. 

Diagnosis. — The presence of the peculiar excavations, the hyper- 
sensitivity of dentin if any, and the acid character of the mucus 
from the follicles, as shown upon test with litmus paper made just 

1 Lectures. 



320 



AFFECTIONS OF THE ENAMEL AND DENTIN 



after rising, 1 are diagnostic signs. Kirk's method of obtaining the 
acid may be used. (See p. 314.) The acid reaction is not marked 



Fig. 304 




— EC 



Sagittal action of human incisor prepared by Hopewell-Smith's process, and stained 
with hematoxylin: E C, erosion cavity, on surface of which can be seen -Baume's 
clefts; P, pulp tissue undergoing degenerative changes; F C, atrophic odontoblasts: 
S D, secondary dentin. X 45. (Hopewell-Smith.) 



Truman. 



EROSION 321 

during the day. The existence of erosion has become a valuable 
diagnostic sign for the general practitioner in his search for the 
nature of masked maladies from which patients frequently suffer. 

Obscure gout has been pointed out through dental indications alone, 
where the practitioner had before been baffled in his diagnosis. 

Treatment. — The treatment of erosion divides itself under two 
heads: Prophylactic and restorative; the prophylactic is again 
divided into local and general treatment. The problem of eradicating 
the cause of the disorder lies in a correction of the morbid glandular 
secretion. It is evident that if the irritation and altered secretion of 
these glands be due to some systemic cause, a disease of suboxidation, 
notably an affection of the gout order, a cure of the local disturbance 
involves the cure of the underlying systemic cause. Talbot 1 reduces 
the acidity to normal with sodium bicarbonate (10 to 30 grains), or 
sodium chlorid (45 grains), after meals; or sodium phosphate morning 
and evening. One-tenth grain of calomel is given each two hours, for 
a time, to cleanse the bowel and stimulate the liver. Eight to ten 
glasses of water should be taken daily. A practically antigout diet 
and hygiene are suggested, to increase oxidation and elimination. 
Local treatment of the gums is necessary. (See pages 97-105.) 

Kirk, 2 working to the end of reducing acid buccal secretion, uses, 
three times a day, y^- grain pure phosphorus in olive oil, in gelatin 
capsules, along with a very mild laxative, and when the urine shows 
a deficiency of phosphates, 25 to 30 grains per diem of glycerophos- 
phate of lime and soda are given. 

Next in importance to the prevention of acid formation is its 
neutralization. This implies the application of alkalies or ^the use 
of alkaline mouth washes. The greatest production of acid occurring 
during the night, applications of adhesive masses of alkaline sub- 
stances are made to the teeth at night. The principal of these is 
prepared chalk, calcium carbonate; it is rubbed over the labial faces 
of the teeth and between them, before retiring. It remains in 
sufficient amount to neutralize any acid substances coming in contact 
with it. 

Excellent results, as to the checking of the progress of the decal- 
cification, are obtained from the use of magnesium hydrate held in 
suspension in water, or milk of magnesia. Kirk found that three 
hours after the use of a teaspoonful of the milk of magnesia, the 
saliva maintained an alkaline reaction. It should be used at night 
as a wash, after cleansing the teeth, the residue to be left as an 
alkaline coating upon the teeth. The chalk and milk of magnesia 

1 Dental Cosmos, December, 1907. 2 Dental Cosmos, 1908, p. 811. 

21 



322 AFFECTIONS OF THE ENAMEL AND DENTIN 

may be mixed into a paste. If the preparation be disagreeable, a 
few drops of essential oil may be added. (See Caries.) The abrasive 
factor and its possibilities as causes of apparent erosions suggest the 
avoidance of any strongly abrasive powders, or, perhaps, a confine- 
ment to the use of castile soap and a soft brush. 

It has been suggested by Ottolengui 1 that in the earlier stages an 
impression and plaster model of the teeth be made for comparison 
at future dates, so that the progress of the erosion may be noted. 

Restorative Treatment. — If the eroded areas be excavated and 
filled, the erosion may proceed about the edges of the fillings. It 
may, however, take some time for the erosion to become as deep as 
the original area. 

If metal be used, the margins must be extended to avoid this, if 
possible. Metal is very unsightly in the locations peculiar to erosion, 
so that porcelain inlays, which the locations favor, are indicated. In 
their place silicate cement fillings may be used, but must be constantly 
kept in a good condition of surface or they become unsightly. 

The generally distributed erosions are only amenable to the prophy- 
lactic treatment (except by crowning, when teeth are largely wasted 
away), and slight erosions are best treated in the same manner. If 
a sharp edge be produced it is well to remove it, as lip irritation may 
possibly be a factor in the acid production. 

MECHANICAL INJURY OF THE TEETH. 

The enamel is a material much more brittle and inelastic than the 
dentin, and, therefore, less capable of resisting a parting strain. 
Under ordinary circumstances, however, well-formed enamel dis- 
tributed over sound dentin resists all the ordinary forces brought 
to bear upon it. 

Under abnormal conditions, however, enamel appears to fracture 
readily in two directions: (1) Along the line of the interprismatic 
cement substance between the prisms themselves, and (2) along the 
line of cement substance between the globules. The possibility of 
reference of all cases into one or other class indicates that the cement 
substance is naturally a tissue relatively weak. 

Dentin may apparently fracture in any plane. 

Causes. — The teeth may be mechanically injured by (1) the action 
of abrasion, which mechanically wears away the teeth; (2) by the 
application of undue force during mastication or by the improper 
use of cutting, filling, or extracting implements; (3) by blows of 

1 Methods of Filling Teeth. 



MECHANICAL INJURY OF THE TEETH 323 

some sort, delivered either directly upon the teeth or through forcible 
closure of the jaws, as the result of a shock or blow delivered upon 
the rim of the jaw. 

Aside from blows or bites of sufficient force to break sound teeth, 
it is rare to find teeth fractured without a previously acquired 
weakness in the tooth itself. The causes of weakness are several. 

During the course of abrasion the enamel is worn to a sharp edge, 
which is readily fractured. Oblique splintering occurs in the line of 
cement substance between the globules. The enamel edges become 
ragged and further fracture is imminent. Thread biting produces a 
similar but localized condition (Fig. 308). 

Caries, by removing the natural support of the enamel, renders this 
brittle material subject to fracture in ordinary use. The removal of 
dentin from both the mesial and distal sides of a crown by caries 
— e. g., a bicuspid — renders the buccal or lingual section liable to 
fracture, as the result of a strain delivered between the cusps and 
tending to wedge them apart. This accident is liable to occur in 
proportion to the lessening of the healthy dentin between the cavities 
or beneath the occlusal fissure. An upper incisor so decayed would 
naturally have its labial section fractured away, particularly its 
incisal half. 

The exposure of the dentin of a devitalized tooth to the saliva 
seems to weaken it. 

While these principles are correct, it is surprising to what extent 
enamel undermined by caries may retain its integrity if properly 
supported by an adhesive oxyphosphate of zinc. 

The packing of cohesive gold against frail enamel walls renders 
them liable to direct fracture, or if packed so as to permit leakage 
the wall is further weakened by lactic acid produced upon its under 
surface. Again, the improperly prepared cavity margin may be 
comminuted, a condition favoring the recurrence of caries. 

Gold does not support enamel walls so well as oxyphosphate. If 
built over comparatively frail walls in such a manner as to protect 
them from direct impact, they stand fairly well. Inlays of gold 
serve a useful purpose in this connection. 

Amalgam by its attendant leakage permits gradual weakening of 
frail enamel walls. The use of a cement lining, as in combination 
fillings, is distinctly useful both as a support and prevention of 
leakage. 

Johnson 1 explains fracture after filling, where the enamel walls 
were previously undermined but not fractured, upon the theory that 

1 Principles and Practice of Filling Teeth. 



324 



AFFECTIONS OF THE ENAMEL AND DENTIN 



Fig. 305 



previous to filling, the pain attendant upon mastication brings about 
a temporary disuse of the diseased tooth. After filling, comfort 
ensues, the patient again uses the tooth, and fracture occurs. 

The fractures caused by blows present features of interest. An 
actual splitting off of one of the angular portions of a crown may 
occur, or a fracture may be seen resembling one sometimes seen in 
a pane of glass, the result of a light blow from a stone. 

In the latter case, the cracks radiate from a central crushed spot, 
and may involve only the enamel. A large section of an incisor may 
be fractured away and include the labio-incisal third and all the 
lingual section of the crown and a small, ob- 
liquely fractured portion of the root. This 
results from a blow — the exact opposite 
usually results from occlusal strain. 

Biting upon hard objects has caused the 
fracture of sound bicuspids and molars, the 
line extending mesodistally between the 
cusps, the fracture being oblique or through 
the crown and between the roots. Thus a 
molar or first bicuspid may be divided into 
two sections, each supported by a root or 
roots (Figs. 306 and 307). 

Fracture and repair of enamel after erup- 
tion is not, so far as I am aware, known. 
Cases of fracture and repair of dentin have 
occurred. 

A case of such repair by adventitious (sec- 
ondary) dentin has been recorded by Tomes, 1 
and Fig. 309 illustrates a fracture of the 
root well below the gum line. The root is 
girdled by the line of fracture, but the dentin 
has been repaired, and the attachment is 
firm. The line evidently indicates a repair 
from the pulp side. A case analogous to heal- 
ing of a comminuted fracture of a central has 
been reported. 2 Fig. 310 illustrates a peculiar fracture due to an 
unknown cause. (See p. 326.) 

In a case reported by Val. Macdonald, 3 of a similar fracture, the 
pulp maintained its vitality in both crown and root for two years, 
and until the tooth was extracted. There was between crown and 
root, a growth of soft tissue connected with both the pulp and the 




Fracture of two years' 
standing with pulp vital 
and a lateral tissue growth 
resembling granulation tis- 
sue covering the root face, 
would explain how the 
case, Fig. 309, occurred. 
(Macdonald.) 



1 A System of Dental Surgery. (See Secondary Dentin.) 

2 Watson: Dental Record, May, 1906. 3 Dental Cosmos, January, 1908. 



MECHANICAL INJURY OF THE TEETH 



325 



pericementum, and considered by Macdonald to be pulpal in origin 
(Fig. 305). Maedonald's case would explain that in Fig. 309. 

In an experimental implantation of a dried tooth, filed to fit the 
socket of a previously extracted tooth, union of osseous nature took 
place, and a slight fracture of the root was reunited by osseous 
deposition. 1 



Fig. 306 



Fig. 307 





Oblique fracture. 



Fracture involving the bifurcation of the roots. 



Longitudinal cracks in the enamel of otherwise fairly sound teeth 
occur, the line running from the labial edge of the gum to the incisal 
edge of an incisor (Fig. 308), or from the fissure of a bicuspid along 
the enamel to the summit of a cusp, or from the cervical margin of 
an approximal cavity to the gum margin. 



Fig. 308 



Fig 309 






Abrasion associated with fracture of the 
enamel. 



Root fracture and reattachment by ad- 
ventitious dentin. (From a specimen.) 



These lines probably indicate that force has been applied, sufficient 
to cause a parting of the enamel cap without loss of continuity in 
the 'more elastic dentin. Dryness from mouth breathing may be a 
possible cause of cracks, and the contact of excessively hot or cold 



Mendel Joseph and Dessonville: L'Odontologie. (See Cosmos, 1904, p. 1060.) 



326 



AFFECTIONS OF THE ENAMEL AND DENTIN 



substances has been advanced as an hypothesis, but mostly they are 
found in cases of overworked teeth. In some cases the enamel 
cracks may be very numerous. These cracks take up stains, and at 
times in the preparation of cavities, cause annoyance by centring 
the chisel and perpetuating a defect, necessitating the removal of 
much tooth tissue or the risking of future caries. In one case typical 
of a class of accidents, the root of a second bicuspid was found loose 
and fractured longitudinally (Fig. 310). As its occlusal end was 
firmly embedded in an encircling crown band, and no pins had been 
used, the only explanation seems to be, fracture in preparation, the 
swelling of the guttapercha root canal filling or the expansion of gas. 
Such an explanation could not apply to the fracture in Fig. 311. 

Fig. 310 




Case of root fracture. (See Text.) 



Treatment. — The treatment of fractures involves considerations 
purely operative, and depends upon the nature of the case. Rough- 
ened, abraded enamel margins are best rounded with carborundum 
stones or coarse sand-paper disks, and should be polished. Some- 
times a deep serration must be filled; corners are to be nearly rounded 
or restored to contour by fillings or inlays, or at times the entire 
incisal edge is to be ground away and the tooth drawn down and 
retained until firm. 

In case of an uncompleted tooth root, and the pulp not quite 
exposed, a pure gold, all-metal crown is to be adapted with or without 
grinding, according to the future requirements, and the root com- 
pletion awaited. If necessary, the capping of the pulp may be 
attempted as well, for the same purpose. 

After root formation the pulp may be destroyed if desired. If 
conservation of the pulp be not possible, the pulp may be prepared 
for removal by pressure anesthesia or conductive anesthesia, and the 
root filled. (See Root Fillings.) 

Fractures involving the cementum demand either the removal of 



MECHANICAL INJURY OF THE TEETH 



327 



the loosened piece and the construction of a special crown retaining 
a portion of the natural crown as a base, or the removal of all of the 
natural crown and the mounting of a substitute upon the root, or the 
parts may be banded, or in case of molars an all-metal crown may 
be mounted. In some cases screws or a staple must be placed in the 
roots and the parts restored with amalgam (Figs. 313 to 315). If 
the loosened portion be retained, thin oxychlorid of zinc is to be 
introduced into the joint after appropriate sterilization, and before 
the gold crown or holding device is set. It distributes itself by capil- 
larity, if the joint is slightly opened once or twice. The split piece, 
if of the oblique type, is apt to irritate, and in most cases in time 
cause lateral abscess. It should ordinarily be removed and the part 
prepared as in Fig. 313. Should the pulp be vital at the time of 



Fig. 311 



Fig. 312 




Fracture of portion of upper cuspid, 
cause unknown. (Skiagraph by E. Ball- 
ard Lodge.) 




Fracture with dovetails for amalgam. 
(Evans.) 

Fig. 313 




Oblique fracture of root, with pin and 
amalgam for restoration, ready for 
crowning. (Evans.) 



fracture, it will become inflamed, and should be removed by the 
pressure method if possible. To accomplish this, the parts must 
be lashed together and an occlusal opening made. After devitali- 
zation, the parts may be given a dove-tailed form, and be temporarily 
held together, internally, by amalgam, or a circular band may be 
inlaid in a trephined groove by Cigrand's method (Fig. 316 1 ). The 
cuspid Toot shown in Fig. 314 had an amalgam filling in its mesial 
side until after the cap and band were constructed. A temporary 
crown caused the wall to fracture out, so the plan was devised of 
drilling holes in the root side, tapping them with the How tap and 



1 For certain crowning devices in cases of fracture, see Evans' Crown and Bridge- 
work, and Goslee's Principles and Practice of Crowning Teeth. 



328 



AFFECTIONS OF THE ENAMEL AND DENTIN 



placing iridioplatinum screws on both sides of the pulp canal groove. 
The pin and cap were then waxed slightly, placed in position, amal- 
gam built in and when hard, the wax was melted by heating the 



Fig. 314 



Fig. 315 





Screws placed into a fractured root to 
enable the building up of amalagam 
around a waxed pin attached to a gold 
cap. This root is one of four piers 
of a nine-tooth bridge. 

Fig. 



Staple used to unite portions of a 
fractured root. (Evans.) 



316 




Cigrand's method of trephining a root face and inlaying a metal ring; 
prevent fracture when plain dowel crowns are used. 



ilso useful to 



cap and pin, which were withdrawn. After thorough hardening, 
the bridge-work was proceeded with. Fortunately the root received 
its strain from the lingual side, which was largely intact. The 
requirements vary, and must have due consideration. 



CHAPTER X. 

STAINS OF THE ENAMEL AND DENTIN. 

Certain stains are found upon the surface of the enamel and some- 
times penetrating its substance. The calculus sometimes located 
upon the enamel is not included in this consideration, though the 
calculus itself sometimes becomes stained. So far as they have 
been observed, stains ma}' be divided into those of metallic and 
non-metallic origin. 

METALLIC STAINS. 

Metallic stains are those which are caused by the direct depo- 
sition of minute particles of metal, inhaled by workers in the metals, 
in the organic collections upon the surfaces of the teeth, or taken 
into the mouth in various solutions of drugs. 

Copper.— Miller found that "workers in copper, brass, or bronze 
all presented a green stain upon the upper teeth, showing every shade 
of green and bluish-green up to bluish-purple. The latter color pre- 
dominated in rooms where phosphor-bronze was worked." Attention 
is called to the fact that "trumpeters very often show a discolor- 
ation of the teeth." Similar discolorations are sometimes noted in 
proximity -to copper amalgam fillings. The presence of copper was 
demonstrated in scrapings from some of the stained teeth, imparting 
a characteristic green color to a Bunsen flame. McGeehee 1 notes 
a case of a metal worker whose enamel was stained and the dentin 
as well, the tooth being vital. The presence of defects or spaces 
containing organic matter is evidenced (see p. 352). Bands or wires 
containing base metals, generally containing copper, sometimes stain 
enamel. 

Iron. — "Workers in iron presented stains of a brownish color." 
As pointed out, "the green salts of iron under the conditions found 
in the mouth would become oxidized and brownish in color." The 
administration of iron salts, medicinally, is believed to produce 
black discolorations, iron sulphid being formed. "Iron deposits are 
usual in the border-line between carious and normal dentin." It is 
believed that the brownish spots frequently seen in connection with 

1 Dental Cosmos, March, 1912. 

(329) 



330 STAINS OF THE ENAMEL AND DENTIN 

incipient or arrested caries of the enamel are due to the formation 
of iron salts. Iron or steel in dentin stains black with iron sulphid. 

Manganese. — Manganese was found in the dark colored deposits 
upon the teeth of herbivorous animals, but as yet not upon those of 
man. The investigator stated "that alkaline saliva may be necessary 
to the production of these deposits." Manganese stains may occur 
from the use of potassium permanganate, manganic oxid being 
formed. 

Mercury. — In cases of prolonged mercurial administration the 
deposits (black) upon the teeth may give the reaction for mercury. 
"If mercury and potassium iodid are given together, the green iodid 
of mercury might be present upon the teeth." It is probable in these 
cases that another discoloring substance may form. There is in 
mercurialism more or less gingivitis; the gums are swollen and 
spongy, bleeding readily. "More or less putrefactive decomposi- 
tion of the albuminous matter present upon the teeth occurs, and 
hydrogen sulphid is formed. Reacting upon the oxyhemoglobin of 
the blood, sulphomethmoglobin is formed — greenish red in concen- 
trated, green in dilute solutions." Miller ascribes the discoloration 
found in conditions of gingivitis from various causes, with lack of 
hygienic care, to a probable reaction between hydrogen sulphid and 
oxyhemoglobin. 

Lead. — Hirt (quoted by Miller) found in cases of lead poisoning, 
discolorations upon the teeth: dark brown at the necks, light brown 
on the crowns, with sometimes a trace of yellowish green. Miller's 
tests (limited in number) showed no lead reaction from the dental 
deposits in lead poisoning. 

Nickel. — Some of the salts of nickel are green. Metallic nickel 
attacked by fluids of the mouth and mixtures of bread and saliva pro- 
duces greenish salts. The entire root of a tooth containing a nickel 
retaining screw has been stained a uniform apple green. 

Silver. — The dentin of pulpless teeth containing amalgam fillings 
is sometimes stained black, owing to the formation of silver 
sulphid. 

The use of silver nitrate as a wash may cause the albuminate of 
silver to precipitate salts of silver upon the teeth. If a cavity be 
touched with silver nitrate and an amalgam filling be introduced, 
the salts of silver will be instantly formed at any point where the 
silver nitrate and amalgam combine. If this be upon the enamel, the 
latter will receive a somewhat lasting black stain. 

The nitrate of silver applied to dentin causes the dentin to assume 
a light yellowish green tinge, and the albuminate of silver is formed ; 
later metallic silver is precipitated, the tissue becoming black. 



NON-METALLIC STAINS 331 

Gold.— Gold chlorid stains may be formed during the bleaching 
of teeth containing gold fillings by the chlorin methods. The dentin 
becomes first pink, then violet or purple, then black. 1 

NON-METALLIC STAINS. 

Green Stain. — The most common of green deposits upon enamel 
occurs upon both the temporary and the permanent teeth, particu- 
larly of young persons. The deposits usually have a crescentic form, 
are mainly upon the labial faces of the anterior teeth, and may be 
but a narrow line or may cover one-half the labial face. It is unusual 
for the deposit to extend far into the interproximal spaces, their 
tendency being to follow the edges of the approximal surfaces. While 
green stain undoubtedly does form upon adult teeth (Figs. 317 and 
318), where clearly the enamel cuticle has long been absent, it is only 
very common upon young teeth where remnants of Nasmyth's mem- 
brane persist about their necks. The color of these deposits varies 
from light green to greenish black. 





Extension of green stain, on the approx- Extension of green stain on the lingual 

imal surface of the incisors. (Miller.) surface of the incisors. (Miller.) 

If an instrument be passed over the portion of enamel affected, 
more or less roughness of the surface is evident. If the deposits are 
subjected to friction with abrasives, they disappear slowly and the 
enamel beneath may be found roughened. This has led to the belief 
that these deposits cause decalcification of the enamel. It is found 
upon adult teeth that when an area of cervicolabial enamel has 
become roughened through slight decalcification, a green stain is 
likely to form upon the rough surface, if proper hygienic care be not 
exercised. It is also found that if the stain be removed by means of 
abrasives, the roughened enamel may be readily polished — i. e., the 
decalcification is very superficial. 

1 Kirk: American Text-book of Operative Dentistry. 



332 STAINS OF THE ENAMEL AND DENTIN 

If cases be observed early enough in childhood, it will be noted that 
green stain is usually preceded by a lack of oral hygiene; collections 
of food debris are not removed from about the necks of the teeth, 
which implies that prior to the formation of green stain the affected 
enamel surfaces have been subjected to the action of fermenting 
food debris — that is, to acids. These facts have led to an acceptance 
of the view that the roughness or decalcification has preceded the 
green deposits. "If teeth be placed in a 10 per cent, solution of 
hydrochloric acid, in from two to four minutes the enamel cuticle 
begins to loosen, and in from five to ten minutes is isolated. It is 
found that the entire stain comes away with the cuticle." 

In even the mouths of children, the removal of green stain with 
pumice may be difficult, showing that some penetration of enamel 
substance has occurred. 

Nature of the Coloring Matter. — The coloring matter is found to 
be insoluble in water, glycerin, alcohol, ether, chloroform, or oil of 
turpentine. Mineral acids, hydrochloric, nitric, and nitrohydro- 
chloric act but slowly upon the coloring matter; even hydrochloric 
acid requires some hours to completely destroy it. Tincture of 
iodin, commonly believed to act as a solvent of green stain, was 
found to affect it but slightly. Both chlorin and nascent oxygen 
destroy the coloring matter rapidly, the cuticle being bleached in a 
few minutes by a 10 per cent, solution of hydrogen dioxid. Thick, 
dark green deposits were incompletely bleached after eight hours' 
immersion in the 10 per cent. H 2 2 solution, pointing to a lack of 
uniformity in the composition of the stain. 

The belief that the green coloring matter is chlorophyl is contra- 
dicted by the fact that it is not soluble in ether. 

Miller 1 regarded the association of the green discoloration with 
sulphomethemoglobin, or some allied substance, as the most probable 
explanation, though he found a micrococcus in a deposit of green 
stain which produced a grayish-green color in glycerin agar. 

Miller did not find any definite connection between a milk diet 
and green stain. 

Goadby 2 has found Bacillus liquefaciens fluorescens motilis present 
in several cases of green stain. It deposits in its culture medium 
a fluorescent blue-green pigment. Other mouth bacteria produce a 
greenish pigment — e. g., Bacillus pyocyaneus and Bacillus fluorescens 
non-liquefaciens. 3 The deposits of green stain are considered to be 
secondary to enamel decalcification rather than the cause of it, 
when found in connection with it. 

1 Dental Cosmos, 1894. 2 Mycology of the Mouth. 

3 Ibid. 



NON-METALLIC STAINS 333 

In case of roughened enamel, green stain appears at times to have 
been taken into its substance, rendering removal without bleaching 
difficult. 

Black Stain. — A peculiar black stain occurs in the mouths of appar- 
ently healthy individuals, both men and women, and smokers and 
non-smokers, and even with those also who drink neither tea nor 
coffee. It occupies the general position described for green stain, 
but may cover much of the surface of the teeth. It occurs in some- 
what unclean mouths, though the teeth may have been regularly 
brushed. As a rule, those teeth having the deposit are comparatively 
free from caries. Its etiology is not worked out, but it may be due to 
a formation of iron sulphid in place of sulphomethemoglobin. It is 
very readily removed, and does not, as a rule, affect the enamel. At 
times a superficial caries is found associated with it, and at some 
minute spot the enamel may be penetrated. Whether this cavity 
is a result of the action of the film is not certain. In a case of a 
woman a black stain was prevalent for years — recently it has entirely 
disappeared. The only available explanation other than some 
possible unknown systemic change, is the use of a well-known tooth 
paste which contains a large percentage of potassium chlorate. 

Tobacco Stains. — Smokers have characteristic black deposits upon 
both the teeth and calculus deposited upon them. The stain is most 
marked upon the lingual surfaces of the teeth, and a pipestem held 
well back in the mouth may cause a thick deposit upon some of 
the posterior teeth. 

Tobacco juice itself stains exposed dentin and cemehtum, and 
enters cracks in the enamel, producing brown discolorations very 
difficult or impossible to remove. McGeehee found tobacco stain 
to have deeply penetrated the enamel tissue. 

Stains Due to Dyes. — McGeehee 1 has shown that colored mouth 
washes containing vegetable or analine coloring matter may stain 
enamel and other tooth structure. The chewing of betel nut or 
other material containing vegetable coloring matter also produces 
a stain characteristic of the coloring element. Dyed cotton also stains. 

Red Stain. — A peculiar red stain occurs upon the necks of some 
teeth, but is not generally distributed. It is probably due to 
chromogenic bacteria, as it is only found on unclean surfaces. 

According to Goadby, 2 Bacillus prodigiosus, Bacillus rouge de Kiel, 
Bacillus mesentericus ruber, Bacillus roseus, Sarcina roseus, Micro- 
coccus roseus, and other micrococci produce a red pigment in at 
least some of their media. 

1 Dental Cosmos, March 1912. 2 Mycology of the Mouth. 



334 STAINS OF THE ENAMEL AND DENTIN 

Sarcina lutea and Sarcina aurantiaca produce yellow and orange- 
colored pigment respectively. 1 The exact relation of chromogenic 
bacteria to stains is not worked out. 



DENTIN STAINS. 

Exposed dentin may be stained as enamel is. In addition it may 
take up certain stains like tobacco. 

Metallic fillings, such as amalgam, containing mercury, silver, 
copper or cadmium metals which combine with sulphuretted hydro- 
gen to form sulphids, may cause staining of dentin. 

Metallic posts containing silver, copper, or nickel, or made of 
steel or iron wire, may produce sulphids in the same manner. The 
dentin may also be stained pink by hemoglobin entering the tubules 
during the progress of venous hyperemia. This finally develops 
iron sulphid. 

The dentin may also be stained by iron sulphid formed during 
putrefaction of the pulp, by the action of ammonium sulphid upon 
the iron contained in the hemoglobin of the blood undergoing 
decomposition. 

TREATMENT OF STAINS. 

Enamel stains are best removed by mechanical means, after the 
removal of calculus from the teeth. (See Salivary Calculus.) For 
this purpose, brush wheels and rubber cups charged with pumice and 
revolved in the dental engine are used to remove the accessible por- 
tions of the stains. Next a wood point, made by sharpening an 
orange-wood stick or hickory shoe-peg to a wedge-shape, is charged 
with the pumice and rubbed by hand over all the surfaces not reached 
by the brushes and cups. For the more inaccessible situations, the 
point is to be mounted in a Jack or other porte polisher. A very fine 
linen tape, a German silver strip, or flat floss silk charged with 
pumice will remove the stains at the contact points. A very small 
finishing bur or dull ordinary No. 1 or No. J bur is useful upon 
lingual surfaces or in grooves. 

The powdered pumice used is best mixed with glycerin, to prevent 
the flying of the pumice during the rapid revolution of the wheels. 
Saturation of the stains with tincture of iodin followed by a douche 
of water renders them more visible, and also brings to view the 
associated bacterial films upon the teeth. 

1 Mycology of the Mouth. 



TREATMENT OF STAINS 335 

Register recommends the use of 1 per cent, hydrogen dioxid, to 

be forcibly sprayed upon the gums and deposits both before and 
after the use of tincture of iodin. The brush and pumice will then 
rapidly remove the stains and bacterial films upon the accessible 
portions of the teeth. 

Tobacco stains in cementum need not be removed to their full depth. 

Head 1 has suggested the removal of deep enamel stains and the 
deposits in irregular depressions and joints of inlays, inaccessible to 
the stick, by the use of nascent oxygen derived from 25 per cent, 
ethereal pyrozone, or a paste of sodium dioxid and water, made by 
dissolving the latter in distilled water at about 32° F. These are 
applied to the part on cotton, and nascent oxygen liberated with a 
hot burnisher. The face and gums are protected by the securely 
placed rubber dam and by oiling the face. 

The method is also applicable to the bleaching of obstinate stains 
of the dentin, especially near the cutting edges. 

In the joints of inlays, fresh cement is to be rubbed — preferably 
the silicates — in order to prevent a rediscoloration. 

If beneath green stains decalcification be discovered, the decal- 
cified area should be polished as well as possible, but not cut away 
unless carious and the patient urged to careful prophylaxis. 

After the removal of calculus and stains from the teeth, the mouth 
and teeth should be kept in as cleanly and aseptic a state as possible, 
by the employment of correct prophylactic measures. Dental caries 
and pyorrhea alveolaris are thus also largely prevented. (See Pro- 
phylaxis of Dental Caries and Pyorrhea Alveolaris.) 

The stains found in the dentin are also divisible into metallic and 
non-metallic. The former are best removed by transforming the 
insoluble metallic salt into a soluble one. 

The most frequent and practicable course is to form soluble chlorids 
through the action of nascent chlorin. Copper, nickel, gold, and 
iron stains should be subjected to the chlorin method of bleaching, 
followed by repeated washings with chlorin water, 50 per cent., and 
hot distilled water to remove the chlorid formed. 2 

Silver stains are converted into silver chlorid by the chlorin 
method, or iodid by the use of tincture of iodin, and dissolved out by 
the use of sodium hyposulphite, followed by hot distilled water. 3 

For mercurial stains Kirk recommends the use of aqueous, ammo- 
niacal solution of hydrogen dioxid after the chlorin method, and a 
saturated solution of potassium iodid after the iodin method, in 
either case followed by washing with hot distilled water. 

1 Items of Interest, 1902. 2 Kirk. 3 ibid. 



336 STAINS OF THE ENAMEL AND DENTIN 

Manganese stain is removable by the use of 25 per cent, aqueous 
solution of hydrogen dioxid, saturated with oxalic acid crystals and 
followed by washing with hot water. 

The non-metallic dentin stains are removable by the use of chlorin 
evolved from chlorinated lime by the reaction with dilute acetic 
acid, or of nascent oxygen evolved from hydrogen dioxid or sodium 
dioxid. 

In either case the color molecule is destroyed by the indirect or 
direct oxidizing effect. 

The hydrogen dioxid may be used in the form of the 25 per cent, 
ethereal solution (25 per cent, pyrozone) applied for a time, or sealed 
within the tooth for twenty-four hours, or the 25 per cent, aqueous 
solution may be driven into the tubuli by the aid of the cataphoric 
current. • 

Sodium dioxid should be employed in saturated solution in distilled 
water (made at about 32° F.). The dentin is first desiccated and 
then saturated with the solution. Weak sulphuric acid (10 per 
cent.) is used to liberate the nascent oxygen. Kirk recommends a 
second application, omitting the use of the acid. 

As with metallic stains, all the by-products should be washed out 
with hot distilled water. 1 

A further description will be given under the caption of Moist 
Gangrene of the Pulp. 

1 For a complete description of the bleaching process, see Kirk's article in American 
Text-book of Operative Dentistry. 






CHAPTER XI. 

DENTAL CARIES: HISTORY; EXCITING AND PRE- 
DISPOSING CAUSES. 

Definition. — Dental caries may be defined as a disease of a tooth 
characterized chiefly by the production of a localized cavity, con- 
cavity, or area containing decalcified tooth structure and due to a 
combined acid fermentation and liquefaction. 

History. — Examinations of crania show the disease to be certainly 
as old as semicivilization, and when more data are obtainable it 
will, no doiibt, be found even older. The skull of a mummy in the 
British Museum, dating 2800 B.C., exhibits well-marked caries and 
other dental diseases. Caries appears in the teeth of the skulls of 
all peoples, no matter what their degree of civilization, provided 
their dietary included cooked, starchy foods. 

Causes. — These may be divided into exciting and predisposing. 

Prior to the investigations of Miller, 1 published in 1882, a vast 
amount of labor was expended in the effort to determine the cause 
of dental caries. The deductions made were partly speculative and 
partly based upon scientific investigations. 

From 1754 to 1835 caries was regarded as an inflammation or 
gangrene of tooth structure; Boudett, Jourdain, Hunter, Fox, Bell, 
Fitch, and Koecker advancing one or the other theory. 2 

In 1835 Robertson, 3 of Birmingham, England, advanced the 
opinion, based upon his observations, that it " is to chemical and not 
to inflammatory action that the destruction of the teeth must be 
attributed." The author pointed out forcibly the errors and fallacies 
of previous writers. He stated that "Particles of food retained in 
fissures and imperfections of the teeth and in the spaces between the 
teeth undergo a process of decomposition and acquire the property 
of corroding, disuniting, and therefore destroying the earthy and 
animal substances of which the teeth are composed." 

John Tomes, a little later, was the first to record microscopic 
examinations of carious dentin. He described the transparent zone 

1 International Dental Journal, 1884. 

2 For an interesting and exhaustive exposition of their views, see American System 
of Dentistry, Section on Dental Pathology, by Black. 

3 A Practical Treatise on the Human Teeth, second edition, Philadelphia,. 1839. 

22 v ( 337 ) 



338 DENTAL CARIES 

lying between the carious and non-carious dentin, and observed and 
pointed out also the dentinal fibrillar. He announced the very 
significant fact in relation to caries, that if blue litmus paper be 
applied to a carious cavity it is at once reddened, which furnishes 
evidence of the presence of an agent capable, if unresisted by the 
vitality of the dentin, of depriving the tissue of its earthy constitu- 
ents, leaving the "gelatin to undergo a gradual decomposition 
favored by the heat and moisture of the mouth. 

Tomes first established the essentially chemical character of some 
features of caries. The character of the acid and its localization were, 
however, not ascertained. 

In 1867 Bridgman promulgated the theory that the crown of the 
tooth and the gum were of different electrical potential, and that 
being bathed in the oral fluids, the conditions of a battery were set up. 

Acid substances were said to be set free at the positive pole (the 
crown), causing decalcification. 

S. B. Palmer, in 1874, claimed that after filling, recurrent caries was 
caused by the conditions of a battery being set up — i. e., the differ- 
ence of electrical potential between the filling and dentin in the 
presence of saliva or of the fluid of the dentin, as an electrolyte 
caused liberation of acids, producing decalcification of the tooth or 
disintegration of the filling — e. g., oxyphosphate. 

Miller, in 1881 and 1900, 1 experimentally examined these assump- 
tions. He ground the enamel away from the crowns of freshly 
extracted teeth and filled cavities made in them with gold and gutta- 
percha. These he placed in separate flasks containing a physiological 
salt solution (0.75 per cent, sodium chlorid). This, in the presence 
of electric currents, should produce hydrochloric acid by liberation of 
hydrogen and chlorin, and decalcification should occur. After four 
years there was no decalcification. 

Similarly filled teeth were suspended in dilute lactic acid. The 
decalcification was exactly similar to that in the unfilled pieces used 
as a control. Had electrolytic currents been generated between the 
metals and dentin, the latter would have been acted upon more 
vigorously than in the unfilled pieces. 

In 1868 Watt 2 advanced the theory that free sulphuric, nitric, and 
hydrochloric acids were generated in the mouth during putrefactive 
processes and caused the different varieties of caries. 

Magitot 3 pointed out that the essential phenomena of caries, as 
they were then understood, were the same in natural teeth mounted 
upon plates as in the natural organs in situ; proving that caries is 

1 Dental Cosmos, April, 1901. 2 Chemical Essays, 1868. 

3 Treatise on Dental Caries, Experimental and Therapeutical Investigations, 



EXCITING CAUSES 339 

intrinsically independent of existence of vitality. By immersing 
teeth in solutions of sugar undergoing fermentative changes, he found 
that decalcification occurred. Teeth immersed in solutions of sugar, 
in which fermentation had been prevented by boiling the solution 
and sealing, or by additions of sufficient carbolic acid, remained 
unaffected. 

Leber and Rottenstein, in 1867, first called attention to the 
probable causative association of bacteria with some phases of 
dental caries. By staining carious dentin with iodin, the dilated 
dentinal tubules were shown to be filled with granular bodies, which 
they recognized as bacteria, identif} T ing but one of the many forms 
of oral bacteria — the leptothrix. They deemed an initial exposure of 
dentin a necessary preliminary to the invasion and growth of the 
leptothrix, which in conditions of lessened resistance gained access to 
the tubules and in some undescribed manner caused their dilatation. 

The question of the recognition of the presence of bacteria directly 
resolves itself into the subject of special staining. Prior to the work 
of Koch, presented in 1881, no means of isolating specific bacteria 
by special cultures and staining w r ere known, and it is remarkable 
that in the same year, the essential features of dental caries were 
first made out with some degree of clearness. 

Miles and Underwood (World's Medical Congress, 1881) pointed 
out clearly and at length, the different appearances produced by 
simple decalcification of dentin and those by dental caries. Speak- 
ing of Magitot's experiments, the}" say: "We assume that two 
factors have always been in operation: (1) The action of acids and 
(2) the action of germs. When caries occurs in mouths it is always 
under circumstances more favorable to the action of germs than to 
the action of acids." They believed that the acids necessary for 
the decalcification were excreted by the germs, which utilized the 
dentinal fibrillar as a food supply. 

It will be seen that the invasion and multiplication of organisms in 
the tubuli were held as the antecedent of the process of decalcifica- 
tion. The deductions of these observers were drawn from data 
not derived from the methods of modern bacteriology — i. e., special 
stains and special cultures. Moreover, they were made before the 
physiological chemistry of bacteria was even partially understood. 

In 1882 W. D. Miller, of Berlin, announced, as the results of 
experiments conducted by him, that he believed the first stage of 
dental caries to consist of a decalcification of the tissues of the teeth 
by acids which are for the greater part generated in the mouth through 
fermentation of carbohydrate food by bacteria. This, it will be 
seen, is a position in agreement with that of Robertson. 

The observations of Miller were supplemented by J. Leon 



340 DENTAL CARIES 

Williams, who demonstrated a microbic collection upon the 
surface of superficially decayed enamel, and having sufficient 
attachment to permit grinding in situ. Williams claimed that 
these plaques are the primary agents which manufacture acid from 
carbohydrate material in association with them. 

These, and other observers whose names will be mentioned in 
place, have thrown side-lights upon the formation and nature of the 
plaque and upon the pabulum which they require and out of which 
they form acid as one of their by-products. 

The reader will be assisted in considering the somewhat discon- 
nected facts hereafter given by bearing in mind the generally accepted 
theory of the modus operandi of caries deduced from the facts brought 
out and which is now briefly stated. The primary cause of dental 
caries is a collection of bacteria upon the surface of the tooth. This 
probably begins with a coating of the tooth by saliva in which a 
certain proportion of solid organic matter exists — mucin, globulin, 
leukocytes, epithelial scales, etc. 

This is immediately infected by ever-present bacteria, which form 
colonies in it. This mass of organic basis and bacterial colonies 
when firmly established can be ground in situ and constitute a 
" microbic plaque." By itself this cannot produce dental caries. 
To this microbic plaque comes the carbohydrate food which is the 
second essential factor in caries. 

This carbohydrate is changed by the bacteria to acid, mainly lactic 
acid. This decalcifies the tooth substance, leaving the organic matrix. 
The organic matrix is next destroyed by bacteria having the power 
of its liquefaction, probably due to their enzymes. Both the inorganic 
and organic bases of tooth structure being destroyed, a cavity is left. 
This being a relatively slow process, the intermediate stages are found. 

There was exception taken to this theory by Miller, who claimed 
that plaque formation was not essential, but that the infected food 
mass could form the acid and act directly. This is simply a question 
of whether bacteria act in the mass or under the mass, and is only 
a question of modus operandi, not of essential fact. Pickerill 1 endorses 
Miller's viewpoint, but so far as the writer is aware neither Miller nor 
Pickerill have offered any satisfactory proof that the plaque which 
von Betist has shown to form in a few hours is not the localizing 
factor. There is, indeed, no reason why an infected food mass should 
not form its own underlying plaque out of there existing mucin and 
bacteria. The theory of self solution of base of attachment of the 
plaque (reason 2 2 ) seems weak in view of the rapidity of bacterial 
reproduction. 

1 The Prevention of Dental Caries and Oral Sepsis, 2d Ed., p. 24. 2 Ibid. 



EXCITING CAUSES 341 

Miller's observations and experiments established the following 
basal facts in connection with dental caries: 

1. That in all cases of dental caries microorganisms may be seen 
under the microscope in the tubules of the carious dentin, and that 
bacteria exist in great numbers in the mouth. 

2. That the invasion of the tubules is always preceded by decal- 
cification of the dentin — i. e., an area, sometimes relatively large, 
of decalcified dentin may be seen in advance of the organisms. 

3. Analysis of the softened dentin proved that a large part of its 
lime salts were removed — i. e., decalcification had occurred. 

4. Test with litmus paper gave the acid reaction in nearly every 
case, so that the inference that decalcification was due to an acid 
was warrantable. 

5. The food substances taken into the mouth are of all classes. 
Carbohydrates (sugars and starches), hydrocarbons (fats), and 
nitrogenous (albuminous) materials. 

The carbohydrates are fermented with acid reaction by many 
mouth bacteria, commonly producing lactic acid; the albumins 
ferment with an alkaline reaction. 

It was inferred from this and other experiments that caries was 
due to the acid fermentation of carbohydrates and not directly to 
the fermentation of albuminous substances. 

6. That oral fermentation is the result of bacterial action, his 
following fundamental experiments show: 

(a) A small tube was filled with a solution of starch and fastened 
to a molar tooth on retiring. The next morning the contents of the 
tube had a. strong acid reaction. A tube of the starch solution with 
saliva added was incubated at blood temperature. After four or 
five hours the mixture became acid. 

(6) The mixture of starch and saliva was kept at 100° C. for a half- 
hour, and incubated. It did not become acid — i. e., the exposure to 
this temperature killed the ferment. 

(c) The saliva was boiled for a half hour and then added to the 
starch solution and the mixture incubated. No acid was produced — 
i. e., the ferment existed in the saliva, not in the starch. 

(d) The ptyalin of the saliva was destroyed by heating the mixture 
for twenty minutes at 67° C; the incubated mixture still became 
acid — i. e. y ptyalin did not act as the acid-forming ferment, but the 
fermentation must have been caused by some other ferment not 
destroyed by exposure to this temperature. 

(e) To the mixture of saliva and starch, carbolic acid was added 
as an antiseptic. No acid was formed, but the ptyalin changed the 
starch to sugar — i. e., the acid-forming bacteria were inhibited, the 
ptyalin not/ 



342 DENTAL CARIES 

(/) A number of tubes were each supplied with a small quantity of 
the saliva-starch solution and sterilized ; a third of them were infected 
from the mouth, a third by carious dentin, and a third were left 
uninfected as controls. The infected tubes became acid; the controls 
did not. 

(g) The first of a series of tubes containing sterilized saliva and 
starch solution was infected with carious dentin; when this became 
acid a fraction of a drop was carried from it to a second tube. After 
that became acid a third was infected from it, and so on indefinitely. 

Conclusion. — Carious dentin contains a ferment or ferments cap- 
able of reproduction — i. e., living organisms are present in it. 

7. The nature of this living ferment was determined by infecting 
a culture medium with carious dentin taken from the deeper layers. 
The bacteria cultivated were distended into pure cultures by carry- 
ing through a series of cultures and examining microscopically during 
the process. The same morphological characteristics were exhibited 
in the last tube, as shown by the germs in the deeper layers of carious 
dentin itself, and were identical with that of Bacterium acidi lactici. 
These germs may be found in the sediment of a culture tube, and 
consist of cocci and micrococci, either single or in chains. These 
cocci possess the power of forming lactic acid from glucose. The 
organism is a faculatative anaerobe (Fig. 319). 

8. A sound bicuspid was sawed into sections, and an equal number 
of these sections placed in each of two test-tubes. Upon these was 
poured a 2 per cent, aqueous extract of beef (albuminous). To one 
tube a minute portion (0.2 per cent.) of cane-sugar was added. Both 
tubes were sterilized, and after cooling infected with a pure culture 
of the germ, obtained from the deeper layer of carious dentin. The 
sugar-containing solution became acid in a few hours; in a week the 
dentin was softened; in two weeks thin sections were completely 
decalcified; in three weeks cavities were found in the dentin, exactly 
similar to cavities formed in teeth in the mouth and presenting under 
the microscope other phenomena of caries to be described later. 

A more prolonged fermentation resulted in the complete disintegra- 
tion of the slabs of dentin, a proof of the fact that one organism may 
completely destroy dentin. 

In the tube containing only the extract of beef, no acid was pro- 
duced, and no decalcification of the dentin occurred. 

From these facts, Miller argued that putrefaction does not initiate 
the process of dental caries, and may not be essential to the destruc- 
tion of either the inorganic or organic dental elements. 

9. That the acid produced was lactic acid, Miller demonstrated 
as follows: 



EXCITING CAUSES 



343 



Starch and saliva were mixed and fermentation induced. This 
was then checked by sterilization with heat. A quantity of material 
being collected in this manner, the whole was concentrated by 
evaporation, and tested with a solution of methyl violet, which 
would turn first blue and then green with an inorganic acid. Not 
so reacting, and not distilling off during the concentration, the acid 
present was pronounced a non-volatile organic acid. The concen- 
trate was shaken with a quantity of ether, which dissolved the organic 
acid present. When the solution was clear, it was filtered and the 
ether partially distilled off, when the partially concentrated solution 
was further concentrated over a water bath and then mixed with an 
excess of freshly prepared zinc oxid. The whole was boiled, water 
being added as needed, until the solution became neutral, when it 
was set aside to crystallize. A drop placed upon a slide under the 
microscope showed the forms of crystals of zinc lactate (Fig. 320). 



\ 






V 



Fig. 319 

\ - \ V 



\ e 



Fig. 320 



QO 



o 
o 



*. 



o j 

\ 




'°(?., 



By testing the molecular weight of the washed and dried crystals, 
it was determined clearly that the substance was zinc lactate. 

In practically a similar manner, lactic acid was obtained directly 
from carious dentin. 

While Miller demonstrated the ability of one organism to produce 
all the essential phenomena of caries, including liquefaction of the 
dentin, he did not claim that only one or two organisms are involved 
in the process, but that " any germs possessing the power of producing 
acid fermentation of food may and do take part in the first stage of 
caries, and that all those possessing a peptonizing or digestive action 
upon albuminous substances may take part in the second stage; 
and that those possessing both properties may take part in both 
stages." 1 

1 Microorganisms of the Human Mouth. 



344 DENTAL CARIES 

He was of the opinion that it is not the presence of this or that 
kind of bacterium, but rather the joint activity of the total flora, 
as expressed in intensity of fermentation in food particles, which 
determines the extent of caries. 

Out of eighteen mouth bacteria examined, Miller found ten that 
produced lactic acid in sugar-containing solutions. 1 He also found 
acetic and butyric acid to be by-products. Miller and others have 
found lactic-acid-producingbacteria plentiful in the mouthsof immune. 

Hinkins and Acree, 2 in experiments upon pure cultures of a number 
of oral bacteria in various artificial media, found lactic, butyric, 
valerianic, formic, carbonic, and hydrosulphuric acids as either 
principal or by-products of the fermentation. 

It is quite clear from Miller's demonstrations that bacteria, or 
at least one bacterium, are the exciting causes of dental caries; and 
that for their function as such they require carbohydrate material as 
food. It is probably true that in order to act, the acid-producing 
bacteria must be attached to the teeth in the form of plaques (to be 
later described), or the food and bacteria as a mass must be attached 
at some undisturbed location. 

The action of bacteria upon these substances has been studied. The 
carbohydrates introduced into the mouth as food are monosac- 
charids, disaccharids, and polysaccharids. (1) The monosaccharids 
or glucoses have the general formula C 6 Hi 2 6 , and are represented by 
dextrose and levulose, found in seeds, fruits, roots, honey, and in 
many forms of candy, such as peanut brittle and glace s, and galac- 
tose formed from lactose or milk sugar by hydrolysis. These ferment 
directly into lactic acid without formation of gas. 

C 6 Hi 2 06 + bacterial enzyme = 2C 3 H 6 3 . 

A certain proportion of the glucose, etc., is appropriated by the 
bacteria as food. (2) Disaccharids or saccharoses have the general 
formula C12H22O11. The principal one is saccharose, found in sugar- 
cane, the sugar-beet, sugar-maple, and maize. This is inverted by 
the ferment of the bacteria into glucose and levulose through a 
process of hydration: 

C12H22O11 + H 2 + bacterial enzyme = C 6 Hi 2 6 = C 6 Hi 2 6 . 

Two other disaccharids enter the mouth or are formed therein: 
lactose and maltose, both C12H22O11 (H 2 0). Lactose exists in milk, 
and by hydrolysis is changed by bacteria to galactose, 2C 6 Hi 2 6 , and 
then ferments like other monosaccharids. Maltose is an intermediate 
product in the formation of glucose from starch, and is produced by 
the action of ptyalin. It is readily fermentable by yeast and by 

1 Microorganisms of the Human Mouth. 2 Dental Cosmos, 1901. 



EXCITING CAUSES 345 

some mouth bacteria (Goadby). (3) Polysaccharids or amy loses 
with the general formula (C 6 Hi O5)n. Starch, cellulose, glycogen, and 
gum. 

Starch was found by Miller not to undergo direct fermentation by 
mouth bacteria — i. e., culture media containing starch, but not 
sugar, when infected by bacteria did not ferment into lactic acid 
unless ptyalin was present. 1 When saliva was used, however, the 
acid reaction occurred, owing to the formation of glucose through the 
action of ptyalin. 

In oral fermentation starch is first changed by ptyalin to maltose 
by hydration, and the maltose to glucose. Then the bacteria change 
this to lactic acid. 

2C 6 H 10 O 5 + 2H 2 + ptyalin = C 12 H, 2 0n(H 2 0). 
Starch. Water. Maltose. 

Erythrodextrin and achrodextrin are said to be associate products. 

C 12 H 22 O n (H 2 0) + ptyalin = 2C 6 H 12 6 . 
Maltose, or Bacterial Enzyme. 

2C 6 Hi 2 6 + bacterial enzyme = 4C 3 H 6 3 . 

In a serial of seven papers in the American Dental Journal, beginning November, 
1910, J. Oxford Keller, D.D.S., endeavors to establish the claim that dental caries is 
produced by causes existing in the saliva apart from organic acids produced by micro- 
organisms. The causes ascribed are: 

1. Neutral salts — a chemical combination of acid and base, as potassium phosphate. 

2. Neutral salt acid or neutral salts with excess acidity. 

3. Neutral salt alkaline or neutral salts with excess alkalinity. 

These by chemism are supposed to extract the salts from tooth structure. 

After making the assertion that lactic acid has never been discovered, even in trace, 
in human saliva, he states that such acids as lactic, sulphuric, muriatic, acetic, oxalic, 
phosphoric, malic, and carbonic may -be contained in saliva in combination or associa- 
tion. (Compare with Miller's determination of lactic acid in carious dentin. — Editor.) 

He states that lactic acid does not develop in the mouth in sufficient strength to 
cause caries; 'that full digestive fermentation necessary to produce lactic acid requires 
from three to six days, and any found would be neutralized by the alkaline saliva. 
(Compare with Miller's Experiment, No. 6, a. — Editor.) 

The editor has carefully read these papers, but can see no reason to disturb the 
text of this work on their account, for the reasons that: 

1. The microbic plaques are always present in enamel in incipient decay, and should 
protect against the access of saliva to enamel. Certainly it would have to contend 
with them, but when the carbohydrate element in it is considered, it is probable it 
furnishes them their pabulum. 

2. That acid may exist in a cavity while the saliva is alkaline, and can be often 
noted in food masses collected on teeth, and can be demonstrated to patients by the 
aid of litmus paper. 

3. That caries is clinically noted in the exact locations in which plaques are found is 
demonstrable with tincture of iodin, whereas if salivary salts are alone responsible 
there is no reason why clean spots should not be affected. 

4. That where saliva is most abundant, decay occurs least, as a rule. 

5. Because the author has by no means shown how the salts of saliva produce 
decay, as his experiments with concentrated saliva, which disintegrated teeth after 
two or three years may have contained concentrated acid, and as compared with 
Miller's experiment No. 8, seems unconvincing. 

6. Black has shown that the plaques formed by saliva in formation of calculus are 
the habitat of bacteria after twenty-four hours, hence their agency is hard to exclude. 
(See p. 349.) 

1 American System of Dentistry, vol. i, p. 805. 



346 DENTAL CARIES 

According to Goadby 1 a few bacteria found in the mouth can pro- 
duce the change direct from starch to maltose and thence to acid. 
This is of no practical consequence, however, as ptyalin is always 
present in the mouth. (See Miller above.) 

Glycogen, C 6 Hi O 5 , or animal starch, is fermented to glucose by 
liver cell ferment, and probably exists in the oral epithelium, in 
certain states as well as in the saliva in others, hence a systemic state 
may introduce glucose (in diabetes). (See Glycogenic Infiltration 
and pages 355, 358, and 359.) 

Miller has demonstrated that bacteria produce acid from starches 
and sugars in about equal proportions, provided the starches are 
cooked. The cooking of starchy foods bursts the starch granules 
and renders them more adhesive to the teeth, as well as more fer- 
mentable. The following synopsis of experiments 2 made with food 
mixed with saliva in definite quantities speaks for itself : 





Duration of 




Material. 


experiment. 


Acids formed in units. 3 


Bread, starch, potato, macaroni, 






rice, corn, and other cooked 






starches 


12 and 30 hours. 


20 to 25 and 42 to 110 


Raw starches, potato, spinach, etc. 


12 and 30 hours. 





Cane-sugar and grape-sugar 


12 and 30 hours. 


17 to 20 and 37 to 41 


Meats, fish, eggs, etc. 


12 and 30 hours. 


or alkaline. 



The table shows that albuminous materials and raw starches 
produce no acid and are not concerned in caries except in so far as 
meats, etc., act as culture media perpetuating bacteria, which later 
may produce an acid reaction in carbohydrate materials. 

Milk contains a carbohydrate (lactose) and often lactic acid bacilli. 
It therefore may supply both the bacilli and their food. This, 
however, has relation to caries only after plaque formation, or by 
retention of acid milk against the teeth. That such a result may 
occur has been shown by Bennett. 

Pickerill 4 tested the acid-forming powers of foodstuffs, chewed, and 
incubated for four days. The following table resulted : 



1 Mycology of the Mouth. 

2 Microorganisms of the Human Mouth. 

3 An acid unit equals the amount of acid necessary to neutralize 0.1 c.c. of a 0.5 per 
cent, solution of potassium hydrate — e. g., if in a quantity of acid material containing 
an unknown amount of acid, 25 of such alkaline units are necessary to neutralize the 
reaction, there were 25 acid units present in it. For purpose of comparison the quanti- 
ties of material used were 4.0 c.c. of saliva and 0.5 grams of the food. 

4 The Prevention of Dental Caries and Oral Sepsis. 



- — Til 



EXCITING CAUSES 347 

Acid units each 
neutralizing c.c. of N/5 
Food material. NaOH. 

Pastry 5.2 

White bread 4.4 

Toast 4.4 

Brown bread 3.6 

Chocolate 3.6 

Biscuit 3.5 

Apple 2.6 

Potato 2.5 

Bread and butter with jam 2.5 

Crust of bread 2.0 

Parsnip 1.7 

Orange 1.2 

Salad 1.1 

Cane-sugar 0.9 

Rice 0.9 

Meat (alkaline to acid unit N/5H2SO4) .... 4.8 alkaline 

He calls attention to the various factors of viscosity of saliva, 
natural adhesiveness of food to teeth, etc., as modifying factors in 
inception of caries. 

Dr. Harold Clark 1 has called attention to the fact that the English, 
whose teeth are much subject to caries, consume chocolate in large 
quantities. The observation of Dr. Albert King (p. 348) regarding 
white bread seems partly confirmed. 

The fats may be fermented with production of fatty acids. Goadby 
has found these of no importance in relation to caries, but Miller has 
shown that the acids found in dermoid cysts, among which are fatty 
acids, can produce decalcification; as other acids were present, the 
relation of fatty acids is not quite clear. Miller asserts that fats 
deposited upon the teeth, as well as calculus retard decay, and that 
fat mixed with saliva will give an alkaline reaction. 2 

That alkalies do not produce tooth disintegration in the mouth is 
shown by the fact that a tooth is not affected by alkaline solutions, 
which are not strong enough to injure the soft parts. 

The influence of carbohydrate diet in the production of caries is 
well shown by tables compiled by Mummery and quoted by Miller. 3 
The races consuming a fish and meat diet almost exclusively — e. g., 
the Esquimaux — are recorded as having about 3 per cent, of caries 
in skulls examined, while those using a mixed or vegetable diet have 
from 10 to 40 per cent, of caries. A most convincing example is 
that given by Miller of two related tribes living on either side of 
the Andes, in the Argentine Republic, and Chili respectively. The 
former, a cattle breeding and meat eating tribe, were practically free 
from* caries, while the latter, living on mixed foods, and consuming 
sugar, had 19 per cent, of caries. Miller and others have shown that 

1 Private communication. 2 Dental Cosmos, 1904. 

3 Microorganisms of the Human Mouth. 



348 DENTAL CARIES 

millers and confectioners rapidly develop caries after engaging in 
the occupation, probably owing to the inhalation of flour and sugar 
dust. Albert B. King 1 has recorded observations upon 132 cases of 
bread eaters, finding that 87 who used bakers' bread exclusively had 
much caries, 31 who used alternately bakers' and home-made bread 
had a less prevalence, while the 14 using home-made bread exclusively 
had only six cavities in three years. The results are certainly worthy 
of attention and of further observations. 

While the fermentation of carbohydrate food debris into acid is 
conceded to be the active exciting cause of dental caries, the modus 
operandi of the inception has not been satisfactorily settled. Miller 
held that as he was able to find bacterial plaques upon many sur- 
faces of teeth, even in the mouths of immunes, without caries beneath, 
the plaques had no relation to the inception of caries of enamel, but 
that the carbohydrate food collecting at favoring spots undergoes 
acid fermentation, with production of enamel decalcification, after 
which the bacteria enter. By experiments, he determined that the 
plaques rather hindered the action of acids experimentally used as a 
decalcifying agent. Black, on the other hand, claims that the bacteria 
produce a gelatinoid material and are left upon the teeth in the 
form of a plaque or zooglea mass, and that the plaque is a thin, 
transparent, slightly yellowish film, not seen without close inspection. 
(It can be stained by iodin. — Editor.) Williams found a film of 
bacteria over the decalcified area in almost all cases of superficial 
caries of enamel, and that it has sufficient resistance to permit 
grinding in situ (Figs. 336 and 337). 

Goadby frequently found on the opaque white patches of softened 
enamel, <a coccus to which Williams called attention, which would 
cause a plaque deposition upon teeth suspended in its culture, and 
that when acid-producing bacteria were mixed with the coccus and a 
carbohydrate medium used, superficial decalcification of the enamel 
under the plaques was produced in from a week to ten days. 

Miller also showed that in the immune with unclean teeth, the 
putrefactive reaction was the dominant one, and that the collection, 
if persistent, could act as a protective against the access of acid- 
producing material. 

In the above data we find that the plaques are almost universal, 
even on immune surfaces (Miller), so that their presence on a decal- 
cifying surface is probably true, as claimed by Williams. If, then, 
they are a protection against the acids produced from carbohydrate 
they should protect, but they do not. Secondly, experiments with 
formed acids are not conclusive, as they may be germicidal and 

1 Dental Cosmos, 1905. 



I'ltk'DISPOSING CAUSES 349 

the dead film might be a relative protection against decalcification 
by the acids. Thirdly, the bacterial films, if containing acid-pro- 
dncing bacteria, can easily take up any carbohydrate food collected 
against them, form acid from it, which they then pass to the enamel 
in a nascent state, hold it against it, and permit it to abstract the 
calcium salts, which they then pass out as lactates, etc., or allow to 
remain in situ. This latter conclusion in the main is the theory of 
Black, and while the decalcifying ability of infected carbohydrate 
food without the intervention of a definite previously formed plaque 
(but possibly by a self-formed one) is a possibility, it seems a reason- 
able conclusion to admit the activity of the plaques. Kirk has shown 
that the precipitation of mucin from saliva rich in mucin content, 
by lactic acid produced by lactic acid bacilli, plays a part in the 
development of the plaques, or by binding the bacteria together 
creates a bacterial plaque. Von Beust 1 has shown that within three 
hours, a mucinous deposit containing many colonies of bacteria which 
rapidly increase in size, may be formed. He attributes to bacteria, 
a large share in the formation of calculus which is the theme of his 
paper, but it also throws light on caries plaques. 

The frequent disturbance of the plaques by monthly cleansings 
(prophylaxis), also prevents dental caries in large degree, so that they 
must have some relation to the inception, though it is only fair to 
state that a constant warfare against any species of bacteria doubtless 
vastly reduces their number in the mouth. 

Noyes' 2 claims that in well-cared-for mouths the confinement of 
acid under the plaques is great, while in uncared-for mouths, though 
much acid -is formed, it may be dissipated in the saliva and the teeth 
not be much attacked. This argument, however, does not take into 
consideration the idea of Miller, that stagnant materials take on a 
putrefactive reaction after the acid production is exhausted (see 
p. 361). 

The Predisposing Causes of Caries. — The causes of the predis- 
position to caries are local and general. 

Local Predisposing Causes. — So invariably does caries begin in 
sulci or pits upon approximal surfaces, about defective fillings, and 
upon unclean surfaces, that faults of form or retentive nature of 
approximation, defects, and faulty position of the teeth must bear a 
relation to the difficulty of keeping the parts free from accumulations 
of bacteria and carbohydrates. 

These local predisposing causes, as they are called, are simply 
conditions favoring the formation of the bacterial plaques upon the 
teeth and the retention of carbohydrate food. 

1 Items of Interest June, 1912. 2 Ibid., 1909, p. 750. 



350 DENTAL CARIES 

Lack of Oral Hygiene. — This is perhaps the most frequent local 
predisponent of caries. It is, in fact, a factor in the exciting cause 
and its reverse is prophylaxis. Most people either can not or will 
not cleanse the teeth thoroughly, hence their lack of care predisposes 
them to caries. It may not occur, but is liable to do so. Otherwise 
lack of hygiene means the presence of microbic plaques and carbo- 
hydrate food, and these are exciting causes of caries. 

Faults of Form. — Deep pits or sulci in the occlusal surfaces of 
bicuspids or the occlusal or buccal surfaces of molars, or in the lingual 
surfaces of incisors, and occasionally cuspids, or pits upon the cusps 
of bicuspids or molars, or in other unusual situations, are not sub- 
jected to a cleansing friction, and so permit bacteria to form plaques 
in these locations (Figs. 322 to 335). 

The nature of the approximal contact has to do with the inception 
of caries. Teeth are seen in which the approximal surfaces are well 
rounded and their buccal and lingual angles free from approximation. 
Such teeth are usually relatively narrow at their cervices, so that 
these also recede well from the line of contact. A V-shaped space 
is formed, which the gum festoon normally nearly fills. Such per- 
fection of contour is also, as a rule, associated with a perfect organi- 
zation of the enamel structure, in virtue of which the surface is 
smooth. While such teeth may decay approximally, there is much 
less tendency to caries (Fig. 338). 

Opposed to this, approximations exist of a broad nature. Broad 
approximations are very common, and not infrequently are asso- 
ciated with a certain degree of enamel opacity and an unevenness 
of enamel surface plainly visible to the naked eye (see p. 352). 

The fluid exuded by the gum is normally alkaline in character, 
and probably neutralizes the products of acid fermentation. In view 
of this fact, the first-mentioned form of contact evidently affords 
more of this immunizing principle. The extension of cavity margins 
beneath the gum has been strongly indicated by experience as good 
practice, and probably is explainable upon the same ground. There 
is also some evidence that the gum has some cleansing action (prob- 
ably phagocytic) upon metal placed beneath it, as it is noted that 
when unclean gold crowns are removed the portion extending beneath 
the gum is usually quite clean. 

With the narrow approximations, saliva is readily forced between 
the teeth and neutralizes the acids formed, or washes away soluble 
carbohydrates, the food for the bacteria. With the broad approxima- 
tions such a result is less likely to occur. 

Stagnant saliva retaining carbohydrates, probably will develop an 
acid reaction. (Miller.) 



PREDISPOSING CAUSES 351 

A depressed approximal surface may decay, but frequently does 
not. An acquired fault of form requires notice. 

Anatomically, the gum covers the cementum and the enamel 
margin. When recession of the gum occurs, the cementum is left 
exposed and food debris accumulates at the angle formed by it with 
the gum. Owing to the cementum being less smooth than enamel, 
microbic plaques readily collect, hence decay of the cementum 
frequently occurs, and is apt to progress rapidly, owing to the 
natural low percentage of inorganic matter (Figs. 321, 332, and 364). 

Arrangement and Position of the Teeth. — The overlapping 
of one tooth upon another creates a form of contact, producing a 
tendency to decay at that point. Angle 1 claims to have observed a 
comparative freedom from caries of very irregular teeth (Fig. 335). 

The presence of a supernumerary third molar, lying at the buccal 
side of the interdental space, between the second and third upper 
molar, or an inlocked bicuspid, very frequently causes approximal 
caries at the contact points. The upper third and lower third molars 
frequently stand in bad relation to the cheek or the gum. 

Food collects upon their buccal surfaces, or they are not subjected 
to the friction of the tooth-brush, and decalcification of a broad area 
of a buccal surface frequently results. 

Defects about Fillings. — Under the caption of Recurrence of 
Caries, will be found a list of the causes which perpetuate caries about 
fillings. Defectively cemented bands are also a cause. I believe 
the abundance of these and a lack of oral hygiene to be, in a large 
degree, the measure of a tendency to persistent caries. A patient 
has a large number of cavities due to a period of negligence, with 
consequent intensity of oral fermentation. If these are obliterated 
in the best manner with physically perfect fillings, and oral hygiene 
be exact, the tendency to caries is largely obliterated. If, on the 
other hand, a large number of even slightly defective fillings are 
made, not only is recurrent caries induced, but the caries ferment is 
continuously active, and exact oral hygiene is an impossibility. The 
number of cleansings a day is no guarantee of perfect hygiene, even 
with perfect teeth, as nothing is more common than to see unclean 
embrasures easily taking the stain of tincture of iodin even in the 
anterior part of the mouth (in less degree than shown in Fig. 321). 
Unquestionably, food debris may even be swept into the interdental 
spaces by brushing alone. Miller 2 has shown that a mixture of bread 
and saliva may become decidedly acid in one hour, and superficially 
decalcify sections of dentin in five hours. With this going on, day 

1 Dental Cosmos, 1903. 2 Ibid., 1905. 



352 DENTAL CARIES 

after day, in cases of soluble teeth and without other aid than 
brushing, and often this not thoroughly done, the persistence of 
decay is not surprising. This, however, does not prove the absence 
of systemic susceptibility or immunity, as an added cause of caries 
or its absence. A condition similar to a defect about a filling, is 
that of the presence of an orthodontic appliance which may afford 
convenient nooks for caries, fungi, and food. In the use of base 
metal wires about teeth for pyorrhea, the wire either has some anti- 
septic, action probably due to the contained copper, or the pyorrhetic 
condition itself furnishes an alkaline element. In such case caries 
frequently does not occur. 

Fig. 321 




Caries of enamel about the cervices of many teeth, due to tenacious films collected 
upon them; at first probably neglected, later impossible to cleanse with brush alone. 
(Model by W. A. Capon.) Fairly clean teeth stained with iodin present such an appear- 
ance. (See prophylaxis.) 

Structure. — While the structure of the enamel has no relation to 
the inception of caries, that is, teeth of poor structure may not 
decay, a roughness of the enamel surface, which often accompanies 
teeth of opaque appearance, may act as a favoring condition, 
and after inception of caries, inferior structure and possibly the 
presence of Caush's tubes may permit more rapid disintegration. 
(See p. 243.) x An interesting examination of 16,000 mouths, made in 
Sweden by Forberg (Stockholm), and others by Rose in Baden and 
Thuringia seems to show that there is a relation between the color 
(structure) of teeth and the presence of caries, the following averages 

1 This statement now made in two editions has been further experimentally con- 
firmed by Pickerill (The Prevention of Dental Caries and Oral Sepsis, 2nd Ed.), who 
has shown by rubbing graphite upon the surface, what he terms "imbrication lines," 
which are associated with "calcarine" fissures in some teeth. Those teeth which 
contain many of the lines and fissures are termed "malacotic," while those but 
slightly imbricated are termed "sclerotic." By test, "malacotic" teeth were found 
more soluble in lactic acid solutions than the sclerotic (Ibid., p. 129). A similar 
result was obtained with hydrochloric acid. Malacotic and sclerotic teeth were both 
but little affected after insertion into an orange for a week but the malacotic were more 
affected (Ibid., p. 130). This fact is of importance in prophylaxis (which see). Carbon 
dioxid in strong solution was found to have no effect upon teeth (Ibid, p. 133). 



i 



PREDISPOSING CAUSES 353 

of all ages being observed: White teeth, 14.3 per cent, of caries; 
yellowish-white, 1(>.4 per cent.; yellow, 20 per cent.; grayish blue, 
24.3 per cent. 

According to these observers, 1 in the regions in which the water 
was rich in calcium salts the individuals examined had the yellowish- 
white teeth. Miller's observations confirm this. 

Gautier 2 has found that in young pigs, deficient osseous development 
corresponded exactly to the lack of calcium salts in their drinking 
water. 

Black 3 made analyses of so-called hard and soft teeth, and deduced 
from them the opinion that the hardness and softness of teeth have 
nothing to do with the inception of caries. 

Touching this point, Black 4 instances the case of a man whose 
enamel had always been chalky and as easily cut as a slate-pencil, 
yet who had little caries of the teeth. That some teeth of apparently 
poor structure and defective form do not decay is also a fact of 
common observation, but, as a rule, they go together. 

These observations, together with the foregoing data, regarding 
the inception of caries, point to the now conceded conclusion that 
the caries of teeth is entirely due to the environment of the teeth, 
and in no sense does it arise from within the tooth, and that in so 
far as the cause is active, it is a question of the localization of the 
exciting cause or its factors on the one hand, and the solubility of 
the teeth on the other; and that no amount of cause is sufficient to 
produce it, unless permitted to exert its effect upon special points 
upon the teeth; in other words, it requires localization and time to 
act, though it may in some cases be broadly localized. 

Othek Local Predisposing Causes. — Acids taken in excess into 
the mouth may act as predisponents by causing a roughness of the 
enamel, which invites the formation of the bacterial plaques. A 
course of tincture of ferric chlorid has a bad reputation in this con- 
nection. In the cases observed by the editor, the hydrochloric acid 
in the tincture seemed to have formed roughnesses between the 
teeth, and many large cavities of not unusual form were later pro- 
duced and evidently due to the carious process. Weld, 5 in a series 
of experiments to determine the action of ferric chlorid, found that 
the pure tincture had little effect, while in the dilution of 1 : 5 in water 
it had much; destroying the entire enamel in twenty-four hours. 
Head's observations on the effect of dilute acids are in general accord 
with this principle (see p. 314). This fact indicates the prompt 

1 Dental Cosmos, 1911. 2 L'Odontologie, October, 1910. See Cosmos, 1911, p. 242. 
3 Ibid., 1898. 4 Ibid. 

5 Quoted by Prentiss, Dental Cosmos, September, 1912, p. 1006. 
23 v 



354 DENTAL CARIES 

local use of an alkali after a dose. (See Prophylaxis of Caries.) 
Howe 1 claims that iron, whether as chlorid or carbonate, taken in 
capsules, returns to the salivary gland for excretion as ferric chlorid 
and may exert injurious effects. 

Morjenstern 2 describes experiments that show that acid iron waters 
or tinctures have a decalcifying action, ferrous iodid and ferric 
chlorid being particularly injurious, while reduced iron, saccharated 
solution of iron, and albuminate of iron produced no ill effects either 
local or through systemic action. 

The acid vomitus of pregnancy and seasickness have an analogous 
effect. It is not likely, however, that during a transatlantic voyage 
large cavities can develop. The probable explanation of the presence 
of such cavities directly after the voyage is that they existed before 
the voyage was begun. Cavities are frequently left or overlooked. 
(See Prophylaxis of Caries.) Since the advent of medication by 
lactic acid preparations and those containing lactic acid bacilli, such 
as sour milk, analogous effects have been observed, and therefore the 
mouth should be washed out with alkaline antiseptics after such 
remedies are taken. 3 

Miller found that the saliva has no antiseptic quality as a whole 
and contains no antiseptic substance, and though he found the saliva 
of immunes to develop a little less acid than that of highly susceptible 
individuals, the difference was not constant and not sufficient to 
account for the marked difference in susceptibility. Miller found that 
carbohydrate foodstuffs mixed with an alkaline saliva became even 
more acid than when the reaction of the saliva was intensely acid 
and the chance for caries was about the same with either reaction 
at the start. Goadby 4 calls attention to the demonstration of Savarelli 
that saliva is germicidal for small quantities of bacteria but loses 
its property with large quantities. This may have some bearing 
on caries. 

Under conditions of oral irritation, such as catarrhal stomatitis, 
or even the presence of many cavities of decay, a stringy, mucinous 
condition of the saliva may result. This may be due to a partial 
coagulation of the mucin by the acid present in the mouth, and the 
coagulum may entangle food masses and cause their adherence to 
the teeth. 

Lack of Saliva of Alkaline Potential. — Pickerill, 5 in exhaustive 
experiments, shows that a continuous flow of saliva may be reflexly 

1 Dental Cosmos, January, 1913, p. 39. 

2 Therapeutische Monatshefte, 1908. 3 Vanel, Dental Cosmos, 1904, p. 694. 

4 Mycology of the Mouth. 

5 The Prevention of Caries and Oral Sepsis, 2d Ed. 



PREDISPOSING CAUSES 355 

excited by foodstuffs having taste and flavor, and especially by 
organic acids of fruit, and argues that such alkaline saliva by flowing 
over teeth neutralizes any acid formed by fermentation. Per contra, 
its absence may be a cause of caries. The argument looks rational, 
but Pickerill has not given any experiments upon susceptible in- 
dividuals to prove his case. 

Very dry mouths have a viscid, tenacious saliva, and usually 
cervical caries is present. Some individuals are greatly incon- 
venienced and may have to frequently moisten the mouth to 
obtain comfort. 

The contention of Lohmann that the carbohydrate element in 
mucin was the cause of caries, Miller examined experimentally and 
found it untenable, but that the explanation here given of its entan- 
gling action is the probable one. He states that very small amounts 
of lactic acid precipitate the mucin and thus enable the bacteria to 
become fixed to the teeth as plaques. 

Miller has noted that some immunes have had exceedingly ropy 
saliva which could be drawn out into long threads, while much 
caries was noted in the mouths of some almost absolutely free from 
mucus. " 

Miller could find no antiseptic quality in the saliva, nor any prin-r 
ciple corresponding to alexin, and found that bacteria developed in 
the saliva of immunes almost as readily as in that of those susceptible 
to caries. 

He also pointed out that the mucus may readily undergo putre- 
factive fermentation with alkaline reaction, and, again, the carbo- 
hydrates entangled in it will ferment with acid reaction, causing any 
caries which might be attributable to mucin fermentation. Gies 1 
has shown that salivary mucin forms viscid films on the teeth, 
which tend to thicken by accretion and in which millions of 
bacteria multiply, particularly at night, when the secretions are 
strongest. 

It is possible that the secretion from the gum may in some cases 
be acid and favor the production of caries by decalcifying the enamel 
about the cervix (Fig. 321). 

Cook has shown that glycogenic infiltration of the oral mucous 
membrane may be produced by the use of irritant or astringent 
washes, which may possibly permit a change of this substance by 
bacteria into acid about the necks of teeth, accounting for a certain 
form of cervical decay long thought to he due to an acid mucus. 
(See Glycogenic Infiltration.) 

1 Journal of the Allied Societies, June, 1912. 



356 DENTAL CARIES 

Systemic Predisposing Causes. — Some individuals seem to 
suffer much from caries; others in less degree. In either case, periods 
of immunity or comparative immunity may be established, and may 
be again followed by a period of susceptibility and a succeeding 
immunity. 

These facts point to the conclusion that a period of caries is due 
either (1) to a temporary lack of oral hygiene with a corresponding 
intensity in oral fermentation — i. e., the exciting cause is active — or 
(2) that it is due to some systemic condition which changes the con- 
stitution of the oral fluids, permitting the formation of the microbic 
plaques upon the teeth, or (3) increases the fermentation by supplying 
some element nutritive to bacteria or (4) depriving it of some element 
inhibiting the growth of bacteria. 

Black has shown that caries fungi are always present in the mouth, 
but do not always form the plaques. Cases also exist in which caries 
has begun during some period of susceptibility and a number of new 
cavities have been started. Later a period of immunity has followed 
and the cavities have not progressed. 

So far as classed, systemic conditions influencing susceptibility 
and immunity may be placed under the four headings: Heredity, 
Prenatal and Postnatal Influences, Age, and Bodily Condition. 

Heredity. — Black 1 records observations on certain families as 
showing a tendency to caries of certain teeth at a given age, or in 
certain positions upon the teeth, e. g., occlusal pits. In certain cases 
the hereditary tendency persists. This tendency must be due either 
to an inherited cell physiology, or diet tendency influencing the oral 
fluid, or to transmitted faults of form or, possibly, of structure of 
the teeth. 

Prenatal and Postnatal Influences. — It is quite probable that 
the systemic condition of the mother during gestation may pro- 
foundly modify the anatomicophysiological condition of the body 
cells of the child; nutritional processes may suffer and the postnatal 
tooth development proceed irregularly, structure being affected; 
moreover, the altered biochemical function of the cells may stand 
in close relation to the constitution of the oral fluids, and these in 
turn may favor the development of caries fungi. If, therefore, the 
mother is not properly nourished, the teeth may not be well con- 
structed, especially if lime be lacking in her food. The same line of 
argument may be applied to bottle feeding of recently born infants, 
or to other conditions profoundly affecting general nutrition. In 
this connection, the absence of the influence of the internal secretion 

1 Dental Cosmos, 1904. 



PREDISPOSING CAUSES 357 

which should be transmitted from mother to child by way of the 
milk, may in the future be shown to have a bearing upon cell develop- 
ment and consequently upon the product (as the enamel). 

In an examination of school children, Th. Frick 1 (Zurich) found a 
much greater percentage of decay in children that had been bottle- 
fed at between three and six months of age. He performed an experi- 
ment on a litter of six dogs, feeding three on cows' milk and bouillon; 
one of them died, and the others had poorly developed teeth. The 
controls were normal. 

Forberg and Rose 2 have shown that the individuals who drink 
water rich in calcium salts have a smaller percentage of caries than 
those drinking soft waters. Ferrier has observed a coincidence of 
caries and the drinking of boiled water wmich had been deprived of 
calcium carbonate. Whether this effect is due to a better develop- 
ment of tooth structure or is a post-developmental effect is not stated 
in either case. The point brought up by Head, 3 who has shown 
the apparent rehardening of teeth in saliva after partial decalcifica- 
tion by a weak acid, opens up the question here as to w r hether the use 
of calcareous waters after tooth eruption can increase the density of 
enamel. Enamel can be dried, why then not infiltrated by calcareous 
solutions? The question cannot now be answered. Another view 
might be that some of the calcium salts in drinking water come 
back to the saliva eventually, and if abundant may neutralize the 
acidity in plaques, through their alkalinity, by combining with the 
acids formed. 

Age. — That the age has an influence upon caries was noted by 
Flagg. He recorded the ages from five to eight, twelve to twenty, 
thirty to thirty-five, forty-five to fifty, sixty to sixty-five years, and 
senility as periods of decay, while the intervening periods w r ere 
intervals of comparative exemption. 

Black has noted that caries is a disease of youth, most intense 
before adult age, at which time immunity is established, provided the 
teeth have been well and promptly filled and the mouth otherwise 
cared for. In view of this fact, he aims at establishing this immunity 
by close attention to the teeth during youth. 

He records fluctuations in susceptibility not unlike those recorded 
by Flagg, and also points out that some persons pass through the 
ordinary periods of susceptibility and first develop caries in middle 
age. In old age, general recession of the gum is common, and in the 
conditions of debility associated w T ith old age, much caries of cemen- 
tum occurs. The patients are often either unwilling or unable to 
keep the cementum cleansed. 

1 Dental Cosmos, 1901. 2 Ibid., 1899. 3 See p. 315. 



358 DENTAL CARIES 

Repeated examinations of the mouths of school-children show a 
deplorable amount of caries which may, perhaps, be attributable to 
several causes, such as the induction of a lessened systemic resistance 
due to confinement, study, etc., and also to the inhalation of vitiated 
air, which presumably also contains acid-producing bacteria. More- 
over, bacteria of caries may be directly transmitted by kissing, 
common use of drinking cups, pencils, etc. 

Michaels, 1 of Paris, has observed that a the saliva of adolescence 
contains a dextrinic principle (glycogen) susceptible of fermentation 
under the influence of ptyalin in the presence of earthy salts. Lactic 
acid is formed." (See p. 98.) 

Bodily Condition. — It is a matter of observation that such con- 
ditions as pregnancy, typhoid fever, anemia, leukemia, diabetes, 
dyspepsia, nervous exhaustion, and debility are frequently accom- 
panied by or followed by a development of cavities of decay, but 
whether the diseases themselves or a coincident lack of oral hygiene 
act to permit the formation of the microbic plaques has not clearly 
been made out. If oral and dental prophylaxis be practised during 
typhoid fever and convalescence therefrom, the production of 
cavities is much limited, but this does not prove anything. 2 The same 
is true of pregnancy, which introduces an exciting cause (the vom- 
itus), and of glycosuria, which may introduce glucose, or a ferment- 
able substance as claimed by Michael, 3 according to whom it takes 
a red coloration with Nessler's reagent, which passes into a grayish 
blue. Black contends that periods of susceptibility are noted both 
in apparent good and ill health. That apparent health may really 
not be true health is a matter that must be considered. 

This bodily condition is seemingly the key to any change which 
can occur in saliva, or mucus, or oral phagocytosis, to one of which 
must be attributed any possible systemic effect upon caries bacteria, 
which can aid or inhibit their growth or localization. It matters very 
little whether the bodily condition is due to heredity as a general 
modification of cell physiology, to age, or some period of stress, as 
the "change" of the teeth, puberty, growth during adolescence, 
diet, business or family anxieties, the degenerative tendencies of 
advancing age, or to some more acute systemic condition, as typhoid 
fever, diabetes, etc., except in so far as these conditions may intro- 
duce into the oral fluid a substance which may act either (1) as a 

1 Sialosemeiology. See Dental Cosmos, 1900. 

2 A caries susceptible was treated before pregnancy and during lactation for many 
cavities. The value of prophylaxis was finally so impressed upon her that she practised 
it properly. Since then she has had typhoid fever, but no increase in caries: which 
amounts only to about one small cavity a year. 

3 Quoted by Kirk, see Dental Cosmos, January, 1914, p. 5. 



PREDISPOSING CAUSES 359 

direct decalcifying agent (an acid) or (2) as an indirect decalcifying 
agent, by furnishing a food material for the bacteria from which they 
may manufacture acid (a carbohydrate), or (3) furnish a substance 
in the saliva which may glue the germs to the teeth, or (4) take from 
the saliva some substance which normally inhibits plaque formation. 

It was shown under the caption of Erosion, that a very weak acid 
may decalcify more rapidly than a stronger solution, and it has 
been noted that in systemic conditions inducing general acidosis 
(as chronic nephritis or diabetes) there is a tendency to deep decalci- 
fication of cervices of teeth, beginning particularly upon the cemen- 
tum. While by no means proved not due largely to fermentation of 
carbohydrate food by bacterial plaques, as a result of defective 
hygiene, there is, nevertheless, a strong suspicion that the acidosis 
expressed as acidity of saliva has produced the decalcification. There 
is also a probable reduction in the amount of normal sodium phos- 
phates as the result of the general acidosis, and this also found in 
the saliva reduces the controlling quality, which Head has shown 
to exist when a certain percentage of basic sodium phosphate is 
present in solutions having an acid reaction. (See p. 315.) On 
the other hand, in such a condition as diabetes there is not only a 
general acidosis, but also the possible transudation of a glycogenic 
principle into the saliva, which can undergo acid fermentation by 
oral bacteria. 

Michaels 1 states that the constitution of the saliva changes with 
the establishment of various diatheses, and that a physiological 
saliva with the biochemical principles in a state of equilibrium is 
probably -very rare. He states that the most active dental caries is 
found in the mouths of hypo-acid individuals, in whom saline chlorids 
predominate over the acid elements of metabolic waste, reducing the 
acidity of body fluids below normal, and inducing a lessened resist- 
ance to development of infective causes, and that caries is least active 
in the hyperacid individuals, in whom sulphocyanid of potassium is 
more abundant in the saliva. He has also claimed to have found 
glycogen in the saliva of adolescents. (See pp. 98 and 358.) 

Kirk 2 claims that in the caries susceptible, the saliva is alkaline to 
litmus, though it may be acid to other reagents (may be ampho- 
teric). That the alkalinity keeps the mucinous elements in solution, 
and at the same time a substance analogous to glycogen and fer- 
mentable by caries bacteria is transuded by the salivary glands, 
which furnishes the bacteria their pabulum after their fixation in 
plaques upon the teeth. He regards this glycogenic principle in the 

1 Dental Cosmos, December, 1900. 

2 Items of Interest, July, 1902, p. 546. 



360 DENTAL CARIES 

saliva as due to carbohydrate diet in excess of the body's needs 
and its capability of storage as fat; that it enters the blood after 
the glycogenic function of the liver has been exerted and is excreted 
in the saliva. He regards the variations in susceptibility as due to 
variations in carbohydrate diet. 

In a recent article/ the possible influence of the hypophysis 
cerebri upon the presence of an excess of sugar in the blood and of 
this as a possible explanation of caries susceptibility, is treated of 
by Kirk, who, however, disclaims any definite finality at present. 

Pickerill argues that as glycogen is rapidly converted into maltose 
and iso-maltose by ptyalin, glycogen and ptyalin should be chemi- 
cally incompatible. He states that in his examination of the saliva 
of diabetics and those suffering from other disease, no sign of glucose 
has been present. The question therefore calls for investigation 
of saliva from the glands direct, to avoid mouth glucose. 

Gies, 2 conducting elaborate experiments concerning the inhibitory 
effect of potassium sulphocyanate upon plaque formation, concludes 
that it is an excretion having no determined bearing upon caries. 
Both he and Howe 8 found experimentally that it did not inhibit 
bacterial growth in cultures. Howe considers it increases the growth. 
Pickerill 4 seems to have found a different conclusion. The Com- 
mittee on Scientific Research of the New York State Dental Society 
furnish the following tests for it: 

Take 2 c.c. of saliva, to which add 2 c.c. of distilled water, and 
shake thoroughly together. Add 5 drops of iron perchlorid, and 
shake again. 

The presence of sulphocyanate naturally in the saliva is determined 
by the color. 

A straw color indicates little or none. A brick color indicates a 
sufficiency. A wine color indicates abundance. 

The Committee on Scientific Research, of the National Dental 
Association, 5 have devised a colorimetric scale which consists of two 
tubes. In tube A, 1 c.c. of saliva is placed. In tube B, 1 c.c. of a 1 to 
2000 solution of sulphocyanate of ammonia. To each, add 2 drops 
of a 5 per cent, ferric chlorid solution from the same pipette. Add 
distilled water; to be in definite quantities until the color matches 
that of the saliva. Calculation of the dilution of the standard 
solution will give the amount of sulphocyanate in the saliva. The 
observations are introduced, that others may continue the line of 
thought. 

1 Dental Cosmos, January, 1914. 2 Ibid., 1913. 

3 The Journal of The Allied Societies, June, 1912. 

4 The Prevention of Dental Caries and Oral Sepsis. 

5 Dental Cosmos, 1908, p. 1365. 



PREDISPOSING CAUSES 361 

The use of potassium or sodium sulphocyanate internally in \ 
to 1 grain doses, in tablet form, has been recommended as a prophy- 
lactic, but while some claim value it is quite likely that other means, 
such as oral prophylaxis conjoined with it, have had much to do with 
lessened caries and hypersensitivity of dentin, as claimed. 

Potassium sulphocyanate is described as a nerve tonic, safe in even 
10 grain doses. It must not be confused with potassium cyanate, which 
is a virulent poison. 

Kirk has succeeded in altering viscid saliva to a more limpid condi- 
tion, by reducing the ratio of carbohydrate to proteid diet, first cutting 
out carbohydrates almost altogether, then adding them gradually to 
the diet. He cites observations upon asylum children kept upon 
well-balanced rations, as having large numbers of arrested caries. 1 
(See p. 359.) 

Black 2 believes that the condition of the system alters the oral 
fluid, so as to permit the bacteria in it to produce a gelatinoid material 
as a by-product, in one case and not to produce it in another, and 
that when produced, plaques adhere to the teeth in sheltered spots, 
while when not produced no plaques adhere, though a general acidity 
of the oral fluids may be produced. 

Miller, 3 some years ago, pointed out that filthy mouths often do 
not contain carious teeth. He offered the rational explanation that 
the unchanged adhering collections, once their acid-producing capa- 
city is destroyed, can even act as a protection in so far as caries is 
concerned. In experiments on artificial production of caries, Miller 
found that the pabulum of the bacteria needed constant change, 
otherwise- putrefaction resulted and decay ceased. The fact that 
fairly cared-for mouths often contain carious teeth is rather an 
argument in favor of the local etiology of caries, as teeth unbrushed 
after a meal, or, rather, not thoroughly cleansed, as is the rule in a 
vast majority of mouths, contain every necessary factor of caries, 
including a renewal of fresh carbohydrate food for the bacteria. 
As prophylaxis becomes more accurate, mouths usually pass into 
a condition suggesting a condition of immunity. It would seem, 
therefore, that unless some other factor of prophylaxis can be intro- 
duced, the mouth should either be thoroughly cleansed or not at all, 
so far as caries is concerned. 

The whole subject of susceptibility and immunity to caries is yet 
obscure and requires accurate experimental study. 

1 Dental Brief, 1907. 

2 Dental Digest, 1907. 

3 Lecture at the University of Pennsylvania. 



CHAPTER XII, 

DENTAL CARIES: PATHOLOGY, MORBID ANATOMY, 
AND CLINICAL HISTORY. 



PATHOLOGY AND MORBID ANATOMY. 

It is a fact of common observation that caries begins only at 
spots protected from friction or uncleansed. These are in order of 
frequency: (1) Pits, grooves, and fissures in the enamel; (2) approxi- 
mal surfaces just above the contact point; (3) smooth surfaces which 



Fig. 322 



Fig. 323 



Fig. 324 



Fig. 325 




Fig. 326 




Fig. 330 




Fig. 333 





Fig. 327 



# 



Fig. 328 




Fig. 331 




Fig. 334 





Fig. 329 




Fig. 332 




Fig. 335 




from any cause are habitually unclean; (4) necks of the teeth at or 
near the junction of the cementum and enamel (Black) (Figs. 322 
to 335). 

In these situations Williams has demonstrated the fact that the 
oral bacteria, protected from friction, attach * themselves to the 
(362) 



PATHOLOGY AND MORBID ANATOMY 



363 



enamel, forming microbic plaques which are sufficiently adherent 
to permit their retention during the grinding of the specimen for 
microscopic examination. (See Figs. 336, 337, and 338.) Carbo- 
hydrate food debris lodges at the points at which retention is favored, 
and either ferments directly against the enamel, or through the 
medium of the microbic plaque. 

The bacteria in the plaque require food and obtain it from the 
carbohydrate and albuminous materials which come in contact with 
them. From the carbohydrates lactic acid is produced as a waste 

Fig. 336 




Section of normal human enamel, showing thick, felt-like mass of microorganisms 
slightly raised from the surface of the tissue, by pressure of the cover-glass in mounting. 
X 250. (Williams.) 



product. (See Chapter XL) Williams states that it is "highly im- 
probable that the enamel is affected, except in rare and special 
instances by any other acid than that which is being excreted by the 
bacteria at the very point at w T hich they are attached to the enamel." 

This thick mass of fungi also prevents the excreted acid from 
being washed away, so that it exerts its full chemical power upon 
calcific tissue. 

The lactic acid produced attacks the inorganic matter of the 



364 



DENTAL CARIES 



enamel, following first the interprismatic cement substance between 
the prisms, later dissolving the transverse cement substance between 
the globules. The effect is to produce an irregular, roughened sur- 
face of the enamel and to bring into view the structure of the rods 
(Figs. 337 and 343). 

Fig. 337 





Microorganisms of caries attached to enamel on approximal surface of tooth. 

(Williams.) 



The gradual loss of cement substance unbinds the enamel globules, 
which are in turn dissolved and washed away, leaving a depression 
or cavity. 

In the process of enamel dissolution, the bacteria may enter the 
crevices formed by solution of the interprismatic cement substance, 
and by repetition of the process gain access to the dentin (Fig. 346). 

The form of the enamel may be retained until and even after 
decalcification has reached the dentin. Clinically, this is seen as an 



PATHOLOGY AND MORBID ANATOMY 365 

Fig. 338 




Superficial approximal caries of enamel with films; also shows slight approximal 

abrasion. (Miller.) 



Fig. 339 




Budding of spores on the stems of Leptothrix racemosa. (Williams.) 



366 



DENTAL CARIES 



opaque white or discolored spot, resisting the instrument until some 
force is used, when it rapidly breaks down (Figs. 338 and 347). 

A central cavity, or several minute openings, leading to or almost 
to the dentin, is sometimes seen in the general decalcified area. It 
signifies the loss of the organic matter of the enamel, by unbinding or 



Fig. 340 



] 







Thick growth of Lcptothrix racemosa fructification heads from approximal surface of 
tooth, under high magnifying power. (Williams.) 



peptonizing actions. The extraction of an approximating tooth 
permits the film to be rubbed off, or prevents the retention of carbo- 
hydrate media, so that the bacteria cease to be active, and this spot 
may remain indefinitely at this point — e.g., the disease is arrested. 
It may cease spontaneously to develop further, owing to the estab- 
lishment of an immunizing systemic change, even though the teeth 



PATHOLOGY AND MORBID ANATOMY 367 

Fig. 341 




A form of streptococcus found abundantly in mouths where very rapid decay of teeth 
is in progress. X 750. (Williams.) 

Fig. 342 




Scrapings of microorganisms from the approximal surface of a decaying tooth: shows 
the Leptothrix buccalis maxima and the Bacillus bucallis maximus of Miller. X 1500. 
(Williams.) 



368 



DENTAL CARIES 



remain in approximation, and strict prophylaxis will usually arrest 
the advance of the process. 

It is also noted clinically and microscopically that the decalcifica- 
tion is deepest at a spot just above the point of contact, and less 
deep at points buccal or lingual, occlusal or cervical, to this spot, 
and still less at points more buccal or lingual — i. e., it shades off to 
zero lingually, buccally, occlusally, and cervically (Fig. 347). The 
dentin may in such cases be deeply affected. Bacteria growing in 
the spaces from which the interprismatic cement substance has dis- 
appeared, causes detachment of masses of partially decalcified rods 
(Figs. 346 and 348). 

Fig. 343 




Section through human enamel, showing first stages of caries, i. e., solution of inter- 
prismatic cement substance. To be compared with Fig. 177. (Williams.) 



When the entire thickness of the enamel is penetrated and the 
dentin attacked, there is a change in the mode of progress of the 
decalcification, which proceeds along the line of union between the 
enamel and dentin, as w T ell as directly into the dentin (Fig. 347) ; in 
this way the enamel is attacked from its dentinal side (backward 
caries) (Fig. 345). 



PATHOLOGY AND MORBID ANATOMY 



369 



In the ultimate breaking down of the enamel the rods first separate; 
the outlines of the several globules of which the rods are composed are 
brought into plain view; next, the calcified plasmic strings noted in 
enamel formation become evident; and finally, the bead-like masses 
upon these strings are left as the ultimate granular detritus of the 
enamel. 

In cases of rapid enamel dissolution, Williams found streptococci 
almost invariably present; and suggests tentatively that the variety 
of organism may be the factor governing the rapidity of dissolution 
(See Miller, p. 344.) 

Fig. 344 



(Fig. 341) 



■ 








■ 




Hi as 1 


/si 



Section of human bicuspid, showing commencement of caries: a and a 1 , appearances 
caused in enamel and dentin by the acid of decay; b and b 2 , shreds of a felt-like mass 
of bacteria raised from the surface of the enamel; c, a cavity. X 12. (Williams.) 



These are probably the Streptotoccus brevis, of Goadby (Micro- 
coccus nexif er, of Miller) . 

Williams found Streptococcus pyogenes albus and aureus and 
Sarcinea lutea to be acid producers. 

The large cocci and diplococci shown in Fig. 349 were always 
found in the secondary decay of enamel. 

" In the direct caries of enamel, the cavities are lined with leptothrix 
and thread-like forms." 
24 



370 



DENTAL CARIES 



"The Leptothrix buccalis maxima and the Bacillus buccalis 
maximus, of Miller, are nearly always found, the latter more spar- 
ingly" (Fig. 342). 

Fig. 345 




Section of carious tooth, showing appearances of decay in enamel and dentin at the 
line of union of these tissues; the dark spots shown in the enamel and dentin are 
masses of microorganisms. X 250. (Williams.) 



Fig. 346 




Penetration of bacilli between enamel prisms after solution of interprismatie cement 

substance. (Miller.) 



PATHOLOGY AND MORBID ANATOMY 



371 



Some of these bacteria are not acid producers, and it may be that 
if a film is composed entirely of these, they may occupy a field and 
really protect it by excluding acid-forming bacteria. 

" Beneath the felt-like masses of thread forms, and lying in contact 
with the decomposing enamel in direct decay, and also in deep cracks 
and fissures in secondary decay, there is invariably found a short, 
thick bacillus, usually constricted in the centre." (Williams, also 
Goadby.) 

Fig. 347 




Decalcification of enamel without loss of form; a, film. X 35. (Miller.) 



Caries of Nasmyth's Membrane. — Miller 1 demonstrated that the 
enamel cuticle may act as a breeding ground for many forms of 
bacteria^which occupy it, forming a matrix which may retain minute 
particles of food, which in turn aid in acceleration of the progress 
of decay (Fig. 351). 

Caries of Dentin. — The bacteria, after penetrating the substance 
of the enamel, attack the dentin. This presents a different anatomical 
and chemical structure to be acted upon. Beneath the enamel, the 
first layer of dentin is of a composition which permits the bacteria 
to rapidly spread laterally along this zone. They also enter the 

1 Microorganisms of the Human Mouth, 1890, and Dental Cosmos, 1900. 



372 



DENTAL CARIES 



tubules of the dentin, and penetrate by multiplication, toward the 
pulp. A wedge-shaped area of decay is produced (Figs. 347 and 353). 
In all cases decalcification precedes these invasions. At the 
periphery, the tubules communicate freely by their lateral branches 
(Fig. 352), and the lateral spreading of the bacteria by multiplication 
is readily explained. 

Fig. 348 




Cover-glass preparation from scrapings of white, opaque, decaying enamel; the 
cement substance between the rods is seen to be dissolved away, and the crevices thus 
formed are filled with round and oval forms of micrococci and bacteria. Stained by 
the Gram method. X 450. (Williams.) 



It is seen clinically in caries, that a portion of the dentin is abso- 
lutely destroyed and removed, leaving within the tooth a " cavity of 
decay," bounded by dentin and enamel undergoing disintegration; 
beneath this lies dentin less affected, and beneath this, sound dentin 
(Fig. 353). These phenomena require explanation. 

The tubules of the decalcified dentin become packed for a distance, 
with bacteria (Fig. 354). These act upon the organic matrix of the 
decalcified tubule walls. The internal pressure due to multiplication 



PATHOLOGY AND MORBID ANATOMY 



373 



Fig. 349 




Various forms of micrococci and bacteria from decaying enamel. Photographed by 
Mr. Andrew Pringle from Williams' cover-glass preparation. X 1000. (Williams.) 



Fig. 350 




Cover-glass preparations of scrapings from decay of enamel; shows Leptothrix 
bucallis maxima and Bacillus bucallis maximus, of Miller. Stained by Gram method. 
X 830. (Williams.) 



374 



DENTAL CARIES 



distends them so that the lumen is enlarged. At the same time, the 
bacteria excrete a ferment or ferments which cause the wall at first 
to thicken. The dilatation and thickening together cause the com- 



Fig. 351 




Enamel cuticle permeated by bacteria. (1100 to 1.) (Miller.) 
Fig. 352 




Carious dentin, stained with fuchsin to show microorganisms. The section shows 
the condition of the tubules as filled with microorganisms along the junction of the 
dentin with the enamel at a. The tubules are very much enlarged. (1/10 immersion 
objective.) (Black.) 

pression of the decalcified intertubular substance, and the tubules 
assume an hexagonal shape owing to the mutual pressure (Fig. 355). 
The phenomenon is not a vital one, as it occurs in artificial caries. 
(Miller.) 



PATHOLOGY AS I) UOIilill) ANATO 



The bacterial ferment possesses a digestive or peptonizing power, 
analogous to trypsin, and begins to liquefy the inner surface of the 
tubule wall. As it does so, the lumen is further increased and the 




Fig. 353 




Longitudinal ground-section through the crown of an inferior molar of a negro: 
E, enamel; D, dentin; C, cement; p, pulp chamber; a, large decay, from the occlusal 
surface; b, small decay, from the mesial surface; c s, cone of septic invasion and 
discoloration; e, partially decalcified and discolored enamel around the carious cavity; 
z, dark cones; z' , clearer cones; z'p, oldest cones where putrefaction of the tooth cartilage 
begins; c, outer transparent zone, or zone of Tomes; s d, secondary dentin, caused by 
irritation; s' d' , secondary dentin deposited by normal physiological process, recession 
of the pulp. This figure is drawn from a ground and polished section mounted in 
Canada balsam. (Gysi.) 



376 



DENTAL CARIES 



bacteria fill the acquired space. Taking up carbohydrates, lactic 
acid is produced, which combines with the calcium salts of deeper 

tubules and intertubular substance and 
FlG - 354 prepares a path of decalcified tissue for 

bacterial advance (Fig. 356). This de- 
calcified tissue, to all intents and pur- 
poses, becomes a culture medium. 



Fig. 355 



a? 



J0M& 



< ■&<&!*' 



vam 



Carious dentin, showing in- 
invaded tubules and uninvaded 
but decalcified intertubular 
substance. (Miller.) 



O 



Cross-section of decayed dentin: the tubules 
through reciprocal pressure have assumed the 
shape of five- and six-sided prisms. (Miller.) 



This combination of the acid with the calcium salts disposes of 
or neutralizes the acid, which, if accumulated to the strength of 



Fig. 356 




\* 



Section of decalcified dentin partly invaded by bacteria: a, uninvaded zone. (Miller.) 



2 per cent., would cause the destruction of the bacteria, by their 
waste products. (Miller.) Calcium lactophosphate, calcium lactate, 
and magnesium lactophosphate are produced. This point has been 



PATHOLOGY AND MORBID ANATOMY 



377 



illuminated by Pickerill, 1 who placed teeth in a definite quantity 
of a known solution of lactic acid. This at first decalcified the teeth 
rapidly, but after thirty days, fresh teeth placed in the solution for 
twenty days were barely affected thus showing an exhaustion or 
neutralization of the acid. 

Miller experimentally found that the calcium carbonate does so 
neutralize the acid formed by formation of calcium lactate, but 



Fig. 357 



Fig. 35S 




tp ! 's 






'4 



*< 




Liquefaction foci. (Miller.) 



Decayed dentin showing a 
mixed infection with cocci and 
bacilli. X 400. (Miller.) 



the calcium phosphate does not, as it 
develops calcium lactophosphate, setting 
free phosphoric acid, which maintains the 
relative acidity. Experimentally, the addi- 
tion of calcium phosphate to a solution 
of lactic acid did not reduce the decalci- 
fication in pieces of dentin placed in it, 

for the reason named. Howe 2 determined by experiments 'that a 
slight increase in phosphate produces great activity of bacteria in 
a starch or sugar solution, with large and rapid formation of acid.' 
That this is true also of the alcoholic fermentation (yeast) and in 
milk. The presence of chlorids he found to restrain fermentation. 
The bacterial ferments continue to digest the wall of the tubule, 
and a time arrives when they have penetrated its substance. The 
intertubular substance is then removed in like manner. The same 



1 The Prevention of Dental Caries and Oral Sepsis, 2d Ed., p. 22. 

2 The Journal of The Allied Societies, June, 1912. 



:57; 



DENTAL CARIES 



process occurring in adjoining tubules as well, the entire dentinal 
substance in the particular area at the cavity surface is destroyed — 
i. e., liquefied and washed away (Fig. 353, a). A cavity results. 

Occurring at a point beneath the general cavity surface, the 
bacteria in several adjoining tubules destroy their walls and the 
intervening intertubular substance, forming what Miller has called a 
"liquefaction focus" (pi. foci) (Fig. 357). This action proceeds until 
the enamel is undermined and the pulp is exposed. A decalcified 
area always exists in advance of the tubule invasion, sometimes large 
masses being found, though it lessens in quantity as the pulp is 
approached. As the enamel is undermined by the carious process, 
the bacteria and their acids decalcify its inner surface, the process 
proceeding from within outward, and termed "secondary caries," or 
"backward caries," of enamel (Fig. 345). 

The enamel is thus weakened and at the same time deprived of 
dentinal support, and breaks down under stress of mastication. 

Any interglobular spaces in the dentin being filled with transi- 
tional or uncalcified material like the tubule walls are rapidly invaded 
by the bacteria during their progress along the tubules (Fig. 359). 

The character of the organisms in the tubules and the nature of 
the liquefaction seem to depend upon the particular germs present. 

Miller has shown that in the deeper portions of tubules micrococci 
appear to predominate over the rod forms, which are also present; 
although one tubule may be filled with cocci and its neighbor with 
rod forms (Fig. 358). It is only in the more superficial layers that 
the thread forms are found in numbers. 

Goadby 1 has done much interesting work in this direction, and 
offers the following classification of bacteria found in decayed dentin : 

Bacteria of Dental Caries. 



Acid-forming Bacteria. 
Streptococcus brevis 
B. necrodentalis .... 
Staphylococcus albus 
Streptococcus brevis 

Sarcina lutea 

Sarcina aurantiaca 
Sarcina alba (Eisenberg) 
Staphylococcus albus 
Staphylococcus aureus . 

Bacteria which Liquefy Dentin (Decalcified.) 
None isolated as yet 
B. mesentericus ruber 
B. mesentericus vulgatus 
B. mesentericus fuscus . 

B. fervus 

B. gingivae pyogenes 

B. liquefaciens fluorescens motilis 

B. subtilis 

Proteus Zenkeri .... 
B. plexiformis .... 



Deep layers of carious dentin. 



Superficial layers of carious dentin. 



Deep layers of carious dentin. 



Superficial layers of carious dentin. 



Mycology of the Mouth, and Dental Cosmos. 



PATHOLOGY AND MORBID ANATOMY 379 

Goadby states that his experiments show that the bacteria which 
dissolve blood serum also digest decalcified dentin, while those which 
only liquefy gelatin do not digest decalcified dentin. 

His experiments also indicate that of the bacteria found in the 
superficial layers of carious dentin some produce digestive enzymes, 
others acid fermentation, and others have both functions. 

Choquet 1 has confirmed the observation of Miller, Vignal, Gallipe, 
and Goadby that the deeper the portions of dentin examined, the 
fewer species of fungi are found in the tubules, and explains it upon 
the ground that the anaerobic or facultative aerobic organisms in the 
outer layers advance into the deeper dentin, because they are better 
suited to the conditions. Kirk advances the as yet unproven idea 
that these bacteria grow toward the pulp, because that is the direc- 
tion of their food supply, i. e., the juices in the protoplasm of the part. 
In this connection, the demonstration of Goadby that some bacteria 
liquefy decalcified dentin shows that this substance is a food supply. 




■■'/ 



Interglobular spaces filled with bacteria. (Miller.) 

These exact findings are interesting as bearing out the general 
demonstrations of Miller; at the same time, Miller's experiment 
showing absolute dissolution by a single bacterium in pure culture is 
to be recalled. (See page 342.) 

Choquet 2 has shown that dental caries may proceed under fillings 
against sound dentin by the following experiment: 

Artificial cavities were prepared in the incisors of a sheep. In these 
was securely sealed with cement, a small particle of a gelatin culture 
of caries fungi, applied on a sterilized platinum cap. Nine months 
later the dentin had become yellow, slightly decalcified, and the 
tubules penetrated by bacteria. This softened dentin was used to 

1 Microbes of Dental Caries, Dental Cosmos, 1900. 

2 Ibid. 



380 DENTAL CARIES 

inoculate a portion of the medium originally used, and the species 
again cultivated. 

Miller 1 estimated the relative loss of inorganic and organic matter 
in dentin during the process of caries, by weighing and analyzing 
equal volumes of carious and sound dentin from the same teeth. 

The carious dentin had lost about seven-ninths of its weight, 
which was due to the loss of twelve-thirteenths of its original calcium 
salts by decalcification, and two-fifths of its original organic matter 
by liquefaction of its substance. 

Tube Casts. — In the zone of decalcification, in advance of bacterial 
invasion of the tubes, are found rod-shaped bodies or shining granules, 
first described by J. Tomes. They occur in both natural and artificial 
caries, hence it must be inferred that their presence is not the result 
of a vital process. 

The rods do not dissolve in organic acids, but dilute sulphuric 
acid quickly dissolves them. They are unaffected by alcohol or 
chloroform, a proof that they are not composed 
Fig. 360 of fat. Miller regards them as probably calcic 

formations against the tubule wall as a cast of 
the wall, and which become loosened when en- 
largement of the tubule occurs. They have a 
tubular structure, are brittle, and may contain 
a central thread-like filament which may possi- 
bly be the remains of a dentinal fibril. Bac- 
teria may surround them, but do not enter 
them. The granules are probably broken rods. 2 
Tube casts. The data point toward a probability that the 

rods are composed of calcium lactate and cal- 
cium lactophosphate, the result of a combination of lactic acid with 
the calcium salts of the dentin. The resultant salt is probably de- 
posited as a tube cast, as suggested by Miller. 

The Transparent Zone. — Around the zone of decalcified uninfected 
dentin appears a zone of dentin more transparent than the surround- 
ing normal dentin. The zone extends from periphery to periphery 
around the cone of carious dentin (Fig. 353, c). The tubules in this 
area contain granular matter not seen in normal dentin, nor in the 
dentin of dead teeth in the same situation. 3 

Tomes and Magitot both regarded the transparency as an attempt 
made by nature to impede the progress of caries. Walkhoff regards 
it as due to a sclerotic action, the fibrillar upon stimulation producing 
intercellular substance (tubule wall), at their own expense and 

1 Microorganisms of the Human Mouth. 

2 Miller. 3 Ibid. 



PATHOLOGY AND MORBID ANATOMY 



381 



primarily of their offshoots. Black once regarded it as the earliest 
stage of decalcification, but has discarded this idea. Miller advanced 
the following data. 1 

1. Transparency indicates increased homogeneity as opposed to 
the heterogeneity of normal dentin — i. e., the coefficients of light 
refraction are brought nearer together. 




Section from a lower incisor worn on a plate, extensive decay without increase of 
transparency. X 15. (Miller.) 

2. It occurs in living dentin only and is not found in natural teeth 
mounted on plates and decayed in the mouth, nor in secondary caries 
of dentin from the pulp cavity to the periphery, and is, therefore, a 
result of vital action. (Compare Figs. 353 and 363 with Figs. 361 
and 362.) 

3. The tubules have their lumen lessened in diameter in the trans- 
parent areas, an agreement with the position of Walkhoff. 

4. Secondary dentin may accompany the process in contiguity 
with the area; moreover, secondary dentin is translucent. It indi- 
cates a constructive excitation of the odontoblasts, of which the 
dentinal fibrils are prolongations (Figs. 353, Sd). 



Microorganisms of the Human Mouth. 



382 



DENTAL CARIES 



5. Chemical analysis proved that no lime salts had been lost, and 
it was pointed out that a gain in the percentage of salts was unneces- 
sary, as new dentin is necessarily composed of organic as well as 
inorganic matter, wherefore the analysis would not necessarily vary 
from that of normal dentin.' 

6. It is found in connection with abrasion of human teeth in which 
the activity of acid may possibly be an open question, and it also 
'occurs in the worn teeth of dogs, the saliva of which is strongly 

alkaline. 

Miller states that opacity may follow or be associated with trans- 
parency. 1 

Fig. 362 




Secondary caries of dentin, advancing from pulp chamber and therefore occurring 
after death of the pulp. Absence of transparency. X 15. (Miller.) 

The natural conclusion is that the transparency is a form of 
tubular calcification, and that it impedes the progress of caries; that 
it does not succeed, as a rule, is due to the overwhelming action of 
the bacteria. 

In cavities from which the walls are broken away, freely exposing 
the carious dentin to mastication, the carious dentin and its con- 
tained bacteria may be removed by friction (Fig. 367, B). 



Dental Cosmos, April, 1903. 



PATHOLOGY AND MORBID ANATOMY 



383 



In the transparent area, the tubules become obliterated ; a polished, 
discolored surface results, resembling in degree an abraded surface. 
This process is called "eburnation," and is really tubular calcifica- 
tion (which see). In the same tooth a more sheltered border of this 
spot may be undergoing the carious process. Miller records cases of 
badly decayed teeth, in which the process ceased spontaneously and 
the dentin became hard and smooth. 

Pigmentation in Caries. — Pigmentation occurs in caries possibly 
from extraneous substances entering the carious area, possibly from 
the substances formed during putrefaction. 

The slower the progress of the decay, the greater the discoloration. 
The colors vary from light yellow to reddish brown, dark brown, 
and black. 

Fig. 363 




Transparency resulting from cracks in the enamel at a and b. X 20. (Miller.) 



The color is, as a rule, darkest upon the outside of the carious 
dentin, but the pigment may extend through large masses and be 
found staining dentin beneath the caries, hard enough to leave in 
situ. As a rule, this is not the case. 

Black suggests the possible formation of sulphids. Miller has 
found iron almost constantly present in carious dentin. The dis- 
coloration of dentin does not seem to be necessarily due to the 
carious process, as it may be seen in areas of abrasion. In a specimen 



384 DENTAL CARIES 

possessed by the editor, a limited cervical caries caused a growth of 
secondary dentin and an area of tubular calcification. From the 
pulpal surface of the secondary dentin to the area of caries, extends 
a sharply defined area which has a flesh-rose color (Fig. 364). Many 
areas of secondary dentin due to abrasion are stained a dark brown. 

Artificial caries produced in teeth placed in a mixture of bread 
and saliva, and the mixture constantly renewed, was white. If putre- 
faction was allowed to occur, discolorations ensued (Miller). 

The discolorations of carious dentin may be due to the action of 
chromogenic bacteria. Miller isolated from the mouth, an organism 
which he named Bacillus fuscans, and "which, cultivated on the 
surface of nutritive agar-agar, in a few weeks imparts to the medium 
a yellowish-brown cQlor, which gradually darkens and extends 
deeper into the substratum as the age of the culture increases." 

It is significant that the three acid-forming organisms found by 
Goadby, in the deep layers of carious dentin, do not form pigment 
in their artificial media. 

Fig. 364 Fig. 365 




Cervical caries associated with secondary Caries of cementum and dentin com- 

dentin. Area pigmented. pletely encircling the tooth. 

Caries of Cementum. — Caries of cementum occurs when the gum 
has receded, exposing the cementum to the fluids of the mouth. As 
a rule, a triangular depression exists bounded by the thickened gum 
margin, the cementum, and the enamel. This favors the collection 
of the bacterial plaques, and caries follows. The gum may be much 
receded, yet no caries occurs. As a rule, however, recession and 
uncleanliness frequently assure its presence. Especially is this true 
in cases of general recession in aged or debilitated persons. 

The path of bacterial invasion after decalcification, is by way of 
Sharpey's fibers to the lacunse and canaliculi; later the dentin is 
invaded as in the crown. Frequently the form of the cementum is 
largely retained, while the decalcification is deep. 



CLINICAL HISTORY 385 

CLINICAL HISTORY OF CARIES. 

The clinical history of dental caries records the observable phe- 
nomena associated with its inception, progress, and termination. 

Inception of Caries. — Caries begins, after the manner described 
in the pathology, at favoring spots. As a rule, in molars the occlusal 
fissures are first decayed, being often carious in this situation before 
fully erupted. Uninformed parents usually consider the first perma- 
nent molar a temporary one, and frequently neglect it. It moreover 
has often seriously defective fissures, which afford lodgement for 
microbic plaques, which seem to be readily formed because of the 
unhygienic state of the temporary teeth, which are frequently 
carious, and the permanent molars are unbrushed during eruption. 
Xot infrequently a cavity is produced on the mesial surface of this 
tooth by a carious condition of the distal surface of the second 
temporary molar. In other mouths, both teeth are affected alike, 
owing to the nature of the approximation. The relative liability of 
the various surfaces of the different teeth to caries may be averaged 
for a great number of persons, but tables drawn from clinical cases 
may have little application to a particular individual, as peculiarities 
of local predisposing causes and personal habits modify the inception. 
Nevertheless, such tables are exceedingly interesting as showing a 
general relative liability. 

The following is from the U. S. Army report, 70,000 teeth being 
filled. 

Average percentage 
Teeth. of each carious. 

First permanent molars 6.5 

Second permanent molars 5.1 

Upper central incisors 3.9 

Premolars 2.8 

Third molars 2.0 

Upper canines 1.7 

Lower incisors .0.7 

Lower canines 0.5 

The lower anterior teeth are the last of all to be affected, and it is 
common to see the six lower anterior teeth free from caries, years 
after all of the other teeth have been lost. This is attributable to 
the constant motion of the saliva, the presence of calculus, and to 
the mechanical effects of tongue movement, lip movement, and 
mastication. 

In the temporary set, the molars decay much more frequently than 
the incisor teeth, partly because longer retained and partly because 
of the width of their approximations. The pulp is readily exposed 
because of its relatively larger size. 
25 . 



386 



DENTAL CARIES 



Approximal cavities are frequently more broad than deep, and 
present problems of anchorage. 

The Progress of Caries. — The rapidity of progress of caries depends 

upon the intensity of the action of the exciting cause, the structure 

of the tooth, and the nature of the vital resistance offered. The 

exciting cause will act most intensely in mouths ill-cared for, and 

containing much carbohydrate debris, and these conditions being 

equal, enamel of poorer organization and presenting a greater degree 

of solubility, in teeth presenting broad approximations, will be the 

more rapidly destroyed. Caries does not begin, but may spread 

under the gum. 

Fig. 366 





Caries undermining enamel: a, masses of bacteria lining the cavity. X 50. (Miller.) 



Williams has expressed the opinion that, as a rule, the process of 
enamel destruction occupies a considerable period of time, a fact 
which may account for the general lack of caries in the temporary 
teeth until about four or five years of age. 

The decalcified enamel may retain its form for a time after dentin 
decalcification has begun. An opaque spot, often discolored, is 
seen upon the tooth, and is readily broken down by an instrument 



CLINICAL HISTORY 38*3 

before dentin decalcification occurs. If the approximating tooth be 
extracted, the carious process may cease, owing to the removal of 
the bacterial plaque, or a lack of food supply (retention). This result 
may not follow, if the dentin has been invaded before the extraction. 

After enamel destruction at a limited area, caries progresses along 
its inner side and penetrates the dentin. The enamel is undermined. 
The extent of cavity orifice is no certain guide as to the depth of 
penetration. The under surface of the enamel then decalcifies. This 
is backward or secondary decay of enamel, and causes an opaque 
appearance of the undermined enamel. 

Cases are frequently observed, in which the only external evidence 
of caries, in a molar or bicuspid, is a white or bluish-black line marking 
the fissure, and yet the dentin may be deeply and widely penetrated 
(Fig. 367, .4). 

Fig. 367 
A B 




As a rule, however, as the cavity in the dentin enlarges, the enamel 
at the orifice becomes disintegrated, so that the orifice is enlarged 
and more food debris enters to accelerate the process (Fig. 353). A 
deep and wide cavity may thus be formed before the patient is 
objectively or even subjectively aware of its existence. After a 
time, the occlusal enamel boundary of the cavity breaks down and 
food is even more readily admitted. 

It has been noted that if the enamel break away in such a manner 
as to expose the carious dentin to the friction of food masses which 
are not retained and to the access of saliva, the progress of the 
caries is delayed and in some cases ceases altogether. The process 
of eburnation is set up. (See Transparent Zone and Tubular 
Calcification.) (Fig. 367, B.) 

The process is sometimes seen in certain cases in which caries 
has followed the dento-enamel junction, the enamel chipping off 
as undermined, so that almost the entire superficial portion of the 
dentin may be subjected to this process and remain of original form 
and discolored and eburnated. This is "spreading caries." In 
other cases the tubules are followed and the pulp is rapidly ap- 
proached. This is "penetrating caries" (Fig. 345). 



388 DENTAL CARIES 

Caries may progress rapidly for a period, and then receive a check 
to its progress. Teeth previously free from the disease may suddenly 
fall victims to its rapid and widespread progress. No doubt, in many 
of these cases, there are removed from or added to the local oral 
conditions, constitutional influences which deter or favor the local 
development of caries producing bacteria. The editor has the models 
of the jaws of a boy, aged fourteen years, with every tooth but three 
decayed to the gum, and the three teeth contained six cavities. 

Secondary dentin is less readily decalcified than primary dentin. 

The dentin of pulpless teeth is more rapidly invaded after enamel 
decalcification than that of vital teeth, owing to the absence of vital 
resistance. This condition does not necessarily apply to the enamel 
of pulpless teeth. 

While caries appears at all ages from childhood to old age, its 
ravages are most pronounced and its progress most rapid during the 
period of adolescence and early maturity. Its effects are most 
marked between the ages of eight and twenty-five years. As a rule, 
a denture which remains at twenty-five years unaffected by caries, 
remains unaffected or but slightly affected to an indefinite age. To 
be sure, this implies two conditions: (1) That the active causes of 
caries have been in but slight evidence, and (2) that the denture is 
of the highest order. The classes of dentures which escape are per- 
fectly formed and symmetrically arranged teeth, in the mouths of 
patients who lead sanitary lives and care for the teeth, who masticate 
vigorously, and who escape other diseases. Very filthy dentures 
may escape, owing, as stated, to putrefaction. (See p. 361.) 

Caries beginning at the junction of the cementum and enamel of 
the teeth has a somewhat different clinical history from that noted 
when its occurrence is in other situations. Its progress is subject to 
great variations. In any of the catarrhal conditions or atrophic 
conditions of the gum which lay bare the neck cementum, caries 
usually occurs. It occurs also as a process secondary to labial 
abrasion and erosion of the teeth. Teeth affected by erosion, however, 
at the ended area are commonly exempt from dental caries. 

The Terminations of Caries. — After the pulp is exposed, it sooner 
or later becomes inflamed and hypertrophies or dies. In the latter 
case putrefaction results, which for a time may exert a restraining 
influence upon decay, but not for a long time. 

Masses of food freely enter the pulp cavity and caries proceeds in 
the dentin from within toward the periphery. This is "secondary 
caries" of dentin, and as it occurs in dentin without vitality, no 
transparency results (Fig. 362). Notwithstanding, caries at this 
stage proceeds rather slowly, particularly if the crown be much 



CLINICAL HISTORY 389 

broken down. The result of secondary caries is a hollowing out of 
dentin of the root, and finally a decalcification of the cementum, 
which may persist for some time as a thin, elastic wall. Finally this 
is destroyed either at the occlusal periphery, or caries causes pene- 
tration to the pericemental tissue. This may occur laterally or 
through to the bifurcation of the roots. In either case it is called 
"perforation by caries." Into this perforation the pericemental 
tissue may become protruded by hypertrophy, and the condition 
of hyperplastic or fungous gum be established. Following the 
breaking down of the crown, the blood pressure in the pericementum 
begins an extrusive process, the pericementum becomes thickened, 
and the tooth is somewhat loosened. 

Decay of the root face and interior, and breakage of the cemental 
margins proceed simultaneously with the extrusion, until finally but 
a small discolored bit of the root end lies upon the surface of the 
gum, from which it is removed by some slight force or is extracted. 

The entire process of caries in a tooth may thus extend over a 
period of from ten to twenty years. 

At times the extrusive force pushes a root up sidewise, particularly 
when the tooth has been tipped over before the loss of the crown. 
It may thus be retained in position and attached upon its under side 
for some time. The upper side may be polished by abrasion. The 
exposed end of a root undergoing extrusion is also sometimes made 
smooth by abrasion. A bit of root left in situ after breakage during 
extraction usually undergoes the same process of extrusion, but may 
not decay until it comes under oral influences. Usually a sinus leads 
to such a root, but very rarely the gum may heal over it. 

Such a root may at any time become the source of apical abscess 
or of an intractable neuralgia, the cause being only determinable 
by radiography. 



CHAPTER XIII. 

DENTAL CARIES: DIAGNOSIS, SYMPTOMS. AND 
PROGNOSIS. 

HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS. 

Diagnosis of Dental Caries. 

The diagnosis of dental caries is made through both objective and 
subjective symptoms. The signs are the existence of cavities and 
of softened areas, directly visible or made evident through instru- 
mental means. The symptoms are pains of several degrees of inten- 
sity. The nature and intensity of the pains furnish a guide to the 
depth of the carious invasion, and but an indirect indication of the 
location of the disease. 

Diagnosis by Objective Symptoms. — The presence of the markings 
of superficial decay, decalcified surfaces, or cavities may often be 
detected at a glance or be seen reflected in a mouth mirror. Opacity 
of enamel is usually due to its superficial decalcification or caries 
beneath it, though at times a malformation may exist. Sometimes 
a zinc phosphate lining will cause an opacity resembling backward 
caries of enamel. The discoloration or opacity about a fissure should 
excite suspicion of caries. In the routine examination for cavities, 
sharp, finely pointed explorers bent at various angles are to be passed 
over all the surfaces of the teeth. If the enamel at any point admit 
the point of the explorer, caries is usually present. Fissures are 
sometimes deceptive in this respect. A good rule is to adjudge the 
presence of caries when the point catches slightly as removed. It 
is well to remember in this connection, that an unsuspected adjunct 
fissure will often contain beneath it caries deeper than the central 
point judged defective. 

In the search for approximal caries great care is required, explorers 
with very short points being often necessary, as long points will not 
turn into the cavity owing to the close contact. The ordinary No. 7 
explorer has not a short enough tine. Frequently a cavity may 
only be discoverable from one point of access, so that the approximal 
surfaces should be examined both from the labial and lingual sides. 
In the absence of evident cavities, some force should be applied to 
(390) 



HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 391 
Fig. 3G8 Fig. 369 





Explorer 
for caries. 
(Jack. 1 ) 






Dow electric lamp for mouth illumination, with 
reflectors. Reflector A is jointed to vary the angle of 
reflection. Reflector B is for illumination of the 
fauces. Reflector C is for lateral illumination. 
(Jack. 2 ) 



detect softened spots of enamel. The 
catching of the explorer upon both teeth, 
after it has passed through the interspace, 
often simulates the catch in a cavity. 

Unwaxed floss silk passed over carious 
surfaces indicates a rough surface by 
fraying. It may, however, at times pass 
readily over a cavity easily detected by 
instruments; so that it is not absolutely 
reliable as a test. It also catches on a 
rough filling or protruding filling margin. 
If the short, sharp pain of hypersensitive 
dentin is produced as floss passes between 
the contact points of the teeth, either a 
masked small cavity or a loose filling 
should be suspected, and if not found 
with the explorer or light, a wedge should 
be introduced. 

The strong light of an electric mouth 
lamp transmitted through the teeth ex- 
hibits a cavity as an opaque spot outlined 
upon a pinkish background. It not only 
permits an easy diagnosis, but also affords 
evidence of the depth of penetration. 
Mechanical separators or wedges are at 
times necessary to press apart contiguous 
teeth sufficiently to admit exploring in- 
struments. 



1 American Text-book of Operative Dentistry. 



Ibid. 



392 DENTAL CARIES 

The necks of the teeth should be examined with sharp points, to 
note any softness of the tooth tissues. The margins, particularly 
the cervical and neighboring margins, of every filling should be 
explored to test the integrity of the junction of filling and tooth, 
or any excess or deficiency of filling material. 

The examination should be conducted by one of two systematic 
methods. In one method the occlusal faces of all the teeth are first 
examined in one survey, then the interproximal spaces, and lastly, 
the buccal and lingual surfaces of the teeth. In the other method, 
every portion of each tooth is examined, beginning with a central 
incisor or terminal molar, before passing to the adjoining tooth. Any 
cavity or condition found should be noted upon a diagram for refer- 
ence at sittings. 

Diagnosis by Subjective Symptoms. — Complaints by patients 
that cold or hot, salt, sweet, or acid substances taken into the mouth 
cause unlocalized or partly localized pain, indicate exposed and 
hypersensitive dentin or pulp exposure. Such complaint is to have 
due consideration. Slight pain has also been produced by the 
passage of floss over a minute cavity unexplorable before wedging, 
and is probably due to compression of liquid upon dentine. This 
symptom at the cervix of a tooth indicates hypersensitive exposed 
dentin. 

Pain beginning without the application of special stimuli, is like- 
wise ordinarily connected with caries or its sequelae, and should be 
taken into account. 

Pain produced upon mastication has either the significance of 
pressure on fibrils or pulp, or is a symptom of pericemental irritation. 

Prognosis of Caries. 

If existing caries be promptly treated in youth and a proper sys- 
tematic prophylaxis be employed, its recurrence during youth may 
be largely prevented. At about adult age a fair degree of immunity 
may be expected. In the absence of treatment or prophylaxis, the 
exciting causes seem to become very active, and many teeth may be 
lost from caries or by reason of extraction for pulp and pericemental 
diseases. Extraction itself brings many evils in its train. 

Even advanced caries may be checked by proper filling or crown- 
ing, and if then prophylaxis receive due attention, the prognosis 
for the teeth is generally good; indeed, it seems as though but few 
conditions exist dependent upon caries alone, which are not subject 
to correction by some of the means within the resources of the 
profession. 






HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 393 



Hypersensitivity of Dentin. 

The exposure of dentin to external agencies is so commonly 
followed by an increase in sensitivity, that the condition requires 
description in itself. It is a general condition attendant upon 
abrasion, erosion, and caries, and has a therapeutics of its own. 

The term sensitive dentin applied to this condition is a misnomer; 
all vital dentin is sensitive, and its degree of sensitivity differs 
markedly in individuals; it is only when hypersensitivity is observed 
that the condition becomes pathological. 

Hypersensitivity of dentin may be defined as such a degree of 
sensitiveness of the dentinal fibrils, as interferes with the comfortable 
excavation and shaping of a cavity of decay ; or which, in the absence 
of dental ministrations, causes painful symptoms, as a rule, reflected 
about neighboring parts. 

Causes and Pathology. — Normally the dentin is protected from 
external agencies by the enamel, and in the early stages of gum 
recession by the cementum, though it has been shown that in some 
cases the dentin is not covered by either. (See p. 182.) 

With the removal of these coverings by caries, erosion, abrasion, or 
fracture, the terminal filaments of the dentinal fibrils become sub- 
jected to sudden variations of temperature, ranging from a little 
above 32° F., the temperature of ice- water, to 130° F., that of very 
hot foods or liquids. 

These thermal stimuli at times give evidence of their effect by 
producing painful sensations. The pulp is stimulated through the 
odontoblasts and their relations with the terminals of sensory nerves 
in the pulp, and a degree of vascular overfulness occurs which may 
be denominated mild hyperemia. The effect of these reactions is to 
cause the sensory functions of the pulp to become somewhat exalted, 
and it therefore becomes more responsive to the stimuli. 

Apart from the effect of thermal changes, other substances act as 
irritants. The lactic acid and other bacterial products in the cavity 
of decay, without doubt play a part in exalting the irritability of the 
fibrils. A slightly loosened filling holds the acid in contact, as such 
cases are often very sensitive. Salt, sweet, or acid substances intro- 
duced into the mouth are also evidently irritant, as active symptoms 
follow their application to hypersensitive dentin. 
« Mechanical abrasion or erosion may irritate the fibrils, or at least 
expose them to the action of other irritants. As a rule, however, the 
abraded or eroded surfaces are protected from hypersensitivity by 
the process of eburnation. (See Transparent Zone.) 



394 DENTAL CARIES 

The scraping of necks of teeth with scalers sometimes induces 
exposure of dentin. Within cavities of decay, the hypersensitivity 
is greatest, as a rule, at the dentinal periphery. That at this point 
the dichotomous endings of the tubules present a greater number 
of fibrils to the action of the irritant is quite evident (Fig. 117). 

In cervical hypersensitivity, the cementum or enamel is removed 
by abrasion, erosion, or caries, and the fibrils are exposed. The 
presence of the granular layer of Tomes in this situation, and the 
possibility of this layer containing the expansions of the fibrils, are 
to be considered. 

In certain cases, the irritation excited by the touch of an instrument 
to dentin adjacent to enamel is carried to the pulp by anastomosing 
dentinal fibrils. This was proved by a few cases, of which the follow- 
ing is an extreme one : 

In a central incisor, secondary dentin had filled a portion of the 
pulp cavity (Fig. 370, S D). Caries had subsequently removed the 

incisal portion of this secondary growth and 
FlG - 370 also the dentin containing fibrils leading 

from the pulp cavity to the middle of the 
incisal edge. The application of an ex- 
cavator to dentin in the incisal portion of 
the cavity (at A), the fibrils of which could 
have no direct relation with the pulp, pro- 
duced flashes of pain. This was unmistak- 
ably of the character of hypersensitive 
dentin. 

A professional friend claimed to feel sen- 
indirect transmission of •.• •, • v 1 '±. £ i 

sensation in a case of hyper- ' f ltivity in a cervicohngual cavity of a molar, 
sensitive dentin: s D, sec- in which the filaments had been destroyed 
hyp^ensnivH^' *" by suppuration for one-third of the length 
grammatic.) of the canals. If his contention was true, 

the sensation must have been conducted 
by way of the granular layer of Tomes to the level of the pulp, 
and thence by the fibrils to its substance. (See Fig. 126.) 

Spots of cervical hypersensitivity have been occasionally recorded 
as occurring in teeth, the canals of which have been filled. 

Head 1 records a case in which the dentin bounding the pulp canal 
remained hypersensitive for a year after the pulp was removed. In 
this connection the possibility of the presence of a vital pulp filament 
in the pulp canal, or of irritable apical tissue receiving the impact of 
liquid forced down upon it by a canal probe, or of a pericementum 

1 Dental Cosmos, 1899. 










HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 395 

irritable to touch of any sort, must all have due differentiation. I 
have never seen a case of hypersensitivity of dentin in which some 
filament of pulp was not present, in at least a part of the tooth. 

Dentin cannot become inflamed in the ordinary sense, as leukocytes 
cannot enter the tubules; nevertheless, the irritability of the fibrils, 
like that of other protoplasm, may be exalted (or lessened). It has 
been noted that during excavation of a cavity the irritability is, as 
a rule, greatest at the surface of the dentin — i. e., at the point at 
which irritants are present in greatest amount, and the fibrils most 
numerous. 

With hypersensitivity other functions are increased, and in con- 
ditions producing a constant stimulation, a constructive change may 
occur and the fibrils form tubular substances at their own expense. 
(See Transparent Zone and Tubular Calcification.) 

That the hypersensitivity is primarily, as a rule, a disease of the 
fibrils involved, or of the fibrils and their odontoblasts is shown by 
the fact that occasionally of two cavities in the same tooth, one will 
present a hypersensitivity and another none; again, one part of a 
cavity may be hypersensitive and the rest not so. In other cases, 
perfectly normal dentin is hypersensitive, as noted when the attempt 
is made to reduce a sound tooth for bridge-work, or a sound fissure 
is opened for prevention of decay. 

There have been two theories accounting for the transmission of the 
impulse which is translated by the patient as pain: (1) That a con- 
contraction of the whole cell, fibril and odontoblast, occurs, the sen- 
sory nerve endings being pressed upon in the act — i. e., contraction 
causes a lateral increase in size. (2) That a wave-like motion along 
the protoplasm is set up, causing excitation of the sensory nerves 
and due to the incompressibility of the water. (Gysi.) 

The first is analogous to the contraction of a voluntary muscle 
cell under nerve impulse. The whole muscle cell contracts, though 
the nerve ending is supplied to only a portion of it. 1 This hypoth- 
esis fits the symptoms as excited by both mechanical and chemical 
irritants, while the second theory does not. If the contention of 
Robertson that the odontoblast is connected with the axis cylinders 
of the nerves be true, then the contraction pulls the nerve fibril. 

If Mummery is correct in his statement that nerve fibres enter 
the tubules and end at their subenamel terminals, then even this 
theory must be modified, as the irritation will be direct. The con- 
traction may still be possible. (See p. 181.) 

1 Black: American System of Dentistry. 



396 DENTAL CARIES 

Symptoms. — A certain degree of uneasiness of undefined character 
may at times be noted in teeth containing cavities, but, as a rule, 
pain other than pulp pain is only felt upon the application of special 
stimuli. Of course, the presence of ferments, acids, etc., in a cavity 
are real stimuli. 

The infiltration of acid, salt, or sweet substances into contact with 
a hypersensitive surface is followed by a wave of gnawing pain, 
reflected usually along the course of contiguous nerve filaments. 
While not definitely localized, owing to the fact that the pulp does 
not possess a tactile or localizing sense, the pain may usually be 
referred to a certain part of the mouth. The pressure of an instru- 
ment upon the dentin is attended by a flash of sharp pain, which 
continues for a time, but lessens if the contact be maintained. In 
this test the pain is localized in the affected tooth, the touch of the 
instrument being followed by a recognition of position by the tactile 
organ of the tooth, the pericementum. 

Occasionally, food forced by mastication against a hypersensitive 
surface, such as due to abrasion or caries in a crevice, will produce 
a sharp pain subsiding promptly, and which may not be repeated for 
some time. The mere rubbing together of opposing abraded surfaces 
may cause the symptom, and is more pronounced if a hard sub- 
stance, as grit gets between them. 

Cavities dried for filling usually produce a steady pain, caused by 
dryness and relieved by an analgesic or by filling. 

It is beyond doubt that individuals differ as to the degrees of 
normal dentinal sensitivity; the dentin of one person may be cut 
freely without evidence of marked pain; in another, the touch of an 
instrument to the newly exposed dentin is productive of unbearable 
pain. The difference in degree of irritability is manifested in another 
manner: If a mild sedative — for example, oil of cloves or an obtun- 
dent — be applied to the hypersensitive dentin of one person, it may 
remove the distressing symptoms, but with others it may be necessary 
to employ the most extreme measures to reduce in any degree the 
hypersensitivity. In some cases, the exposure of dentin about the 
necks of teeth may induce such an unbearable local pain or neuralgic 
condition as to positively demand relief. 

In a few cases enamel has exhibited sensitivity. In one case the 
effort to open sound fissures about a cavity for prevention excited 
sharp pain, ceasing upon removal of the instrument. The patient 
was, however, a sufferer from insomnia, and from the effects of 
morphine taken for it, and her dentin was exquisitely sensitive. The 
same phenomenon of enamel sensitivity is to be noted in one of her 
children. 



HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 397 

In another patient, the side of the enamel exposed by a cavity in a 
molar analogous to that in Fig. 370 gave flashes of pain when touched 
with an excavator point, though no evident direct path of trans- 
mission to the pulp could be seen. Caush's tubes and indirect trans- 
mission seem the only basis of explanation. (See Fig. 179.) 

There is a pseudohypersensitivity of enamel in some cases, due to 
apprehension. The patients can be ridiculed out of the idea by 
demonstrating its absurdity, as, for example, by touching a cusp 
and then showing them the part touched. Pericemental irritability 
at times must also be excluded. 



Fig. 371 



Fig. 372 




The Teter nitrous oxide and 
oxygen apparatus on apparatus 
stand. 




Gregg nasal inhaler. 



There can be no question that systemic, nervous irritability from 
any cause aggravates the phenomenon of hypersensitivity, though 
whether it can make dentin more sensitive, or whether the patient 
is less able to endure pain, is not clear. 

The general perceptivity of the individual seems to play a part, 
and even apparently normal dentin may be exquisitely hypersen- 
sitive. Again, pain produced in excavation may be due to the 



398 DENTAL CARIES 

character of the manipulation, heavy continued burring producing 
heat; lighter touches may excavate equally well, but produce much 
less pain. The dulness of the excavator or bur has a similar effect. 

Diagnosis. — In the diagnosis the above characteristic symptoms 
are to be considered. The decisive test is made by pressing an 
instrument upon the suspected surface, when the characteristic pain 
is produced, subsiding upon or shortly after removal of the contact. 

Upon the pulpal wall of deep cavities doubt may exist as to 
whether the pain is due to pulp irritation. 

A suspected exposure may be differentiated by the localization of 
the pain upon touch, to a point corresponding to the pulp horn or 
pulp body, or by the point catching in the exposure. Hypersensitive 
dentin will be more generally distributed or occur at points at which 
exposure is impossible. Pulp abnormality or approach may be 
detected by means of a drop of cool water or a blast of cool air from 
a syringe. (See Hyperemia of the Pulp.) 

Treatment. — The methods of treatment which have been followed 
for the relief of hypersensitivity of dentin, and the induction of such 
a degree of analgesia as will permit the necessary cutting of dentin, 
may be divided into general and local. 

General Remedies. — The general remedies employed are those 
which abolish or lessen the perceptive function in the centres of the 
fifth pair of nerves, or which reduce hyperirritability of the nervous 
system. Either general anesthesia or general anodynes are em- 
ployed to lessen perception. The inhalation of a few whiffs of chloro- 
form or ethylic ether lessens the perception of pain, or a mixture of 
chloroform, ether, and alcohol may be used. Chloroform is usually 
avoided in this connection on account of its dangers when used in 
the sitting position. Slight etherization, the inhalation being carried 
only to the benumbing point, affords marked relief from the 
pain incidental to the cutting of hypersensitive dentin. Nitrous 
oxide and oxygen administered to the point at which "analgesia" 
without anesthesia occurs is a method now much employed. A 
special nasal inhaler admits the gases in various combinations, 
the mixture of the prepared gases being made in the mixing 
chamber of the apparatus, after the gases leave the cylinders. 

It is preferable that the gases be warmed to avoid the irritation 
of the lungs by the cold gases, though for short operations this is 
often omitted. 

Rebreathing the carbon dioxid and gases exhaled is also advocated 
as a respiratory stimulant and for economy. In view of hypersensi- 
tive dentin the method is now routine for cavity preparation and 
for the grinding of teeth with living pulps, for abutments or for other 



HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 399 

work involving a reasonable amount of pain. It is not generally 
useful for pulp removal unless complete anesthesia is induced. The 
method has various dangers which, while not preventing its use in 
careful hands, renders it not to be carelessly employed. Fear is apt 
to contra-indicate its use in children. 

The element of suggestion and confidence on the part of the 
operator seems to play an important part in the success of the anal- 
gesia, though the analgesia is not dependent upon it. The patient 
is able to cooperate with the operator, not having lost consciousness. 
In the practical application of the mixed gases, the apparatus is first 
set as to constancy of flow of both gases, the proportion of 95 per 
cent. N 2 and 5 per cent. O being first applied, until the patient 
reaches a condition of somnolence, of which he informs the operator. 
The proportions are now T changed until approximately 80 per cent. 
N 2 and 20 per cent. O are being given, though this proportion 
is variable. The patient is instructed to breathe through the nose if 
pain is felt, thus obtaining deeper analgesia. Conversely, as work is 
not being done, he may breathe through the mouth. If greater depth 
of anesthesia is required, the exhaling valve which ordinarily vents 
the expirations is adjusted and the patient then rebreathes the 
gases together with his own carbon dioxid, which further stimulates 
respiration and gradually passes into anesthesia, especially if the 
percentage of oxygen be decreased. Without rebreathing, 95 per 
cent. N 2 and 5 per cent. O will produce anesthesia. The amount of 
rebreathing is controlled by a valve. Somnoform has also been used 
with a special inhaler (De Ford or Starck) to produce analgesia. 

The administration of general anodynes, particularly the com- 
bination of morphin and atropin, has been found useful in this field. 

1$ — Morphinse sulph gr. § 

Atropinae sulph gr. r ig 

M. etft. pil. No. 1. 

Sig. — To be taken one-half hour before operation. 

Flagg noted that blondes bear morphin sulphate better than 
brunettes; particularly are nervobilious and bilionervous patients 
idiosyncratically opposed to its use, the physiological action of the 
drug being reversed or the after-effects being pronounced. Patients 
having dark hair and blue eyes may be expected to be thus idio- 
syncratic. For them, he recommended morphin bimeconate solution 
in doses equivalent to J grain of the salt, to be taken one the evening 
before, and the other before the operation. 

1 For details of apparatus and application read C. K. Teter, Dental Cosmos, August 
1912; W. C. Teter, Dental Brief, August, 1911; A. E. Smith, Items of Interest, 
December, 1913; Harold B. Clark, Items of Interest, April, 1914, and others. 



400 DENTAL CARIES 

Chloral in 5 or 10 grain doses, administered in water before the 
operation, has a quieting effect upon the nervous system. Ambler 1 
has suggested the use of from 10 to 20 drops of fluidextract of piscidia 
erythrina, to be administered about ten minutes before operating. 
Drowsiness may be expected. Phenobromate, 10 grains, before 
operation, or 15 grains for any great pain, may be administered in a 
copious draught of water. 

For the reduction of excitement and nervousness in anticipation 
of dental operation, bromural, 5 grs., ordinarily to be administered 
while waiting, or 10 grs. in unusual cases, is highly recommended for 
this purpose by Hecker. 2 It is also useful in insomnia, and its 
associated hyperesthesia. Quinine sulphate, 5 grains a half-hour 
before operation, or better if preceded by another dose the day 
before it has been used. 

Hyoscyamin hydrobromate, -£$ grain, will be useful in those cases 
which are associated with muscular spasm or hysteria. 

The coal-tar derivatives, phenacetin, acetanilid, and others, are 
occasionally efficient. The preparation known as antikamnia (said 
to be a combination of acetanilid, caffein citrate, and sodium bicar- 
bonate) and ammonol (acetanilid and ammonium carbonate, equal 
parts) are to be preferred in this connection. The dose of the latter 
two is 10 grains, administered one-half hour before operation. 

The induction of the hypnotic state belongs in the category of 
means acting upon the nerve centres. The use of the ordinary 
suggestion that the work will not be unduly painful, considerate 
treatment, patience, and the employment of remedies all have a 
calming influence, permitting relaxation upon the part of the 
patient, who, if "keyed up" to expect great pain, will expect and 
feel unduly. 

The use of blue-light anesthesia consists in causing the patient to 
gaze intently for a few minutes at a blue-globed electric light having 
a reflector behind it. A blue veil is thrown about the head and lamp 
to exclude daylight. Short operations have been performed under 
its sedative, or, possibly, hypnotic effects, though it seems to fail 
in some cases. 

Local Treatment. — The local treatment of hypersensitive dentin 
may be considered from two standpoints, according to whether a 
concavity containing it requires excavation, or whether the hyper- 
sensitive spots are not to be excavated after treatment. 

Treatment in Cavities of Decay. — The remedies employed in 
the endeavor to reduce or abolish hypersensitivity in a cavity of 

Dental Cosmos., 1901. 2 Ibid., 1909, p. 844. 



HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 401 

decay at the time of operation are quite numerous; few are, however, 
always effective. They may be classed under two headings: 

1. Those which temporarily benumb or anesthetize the fibrillar and 
prevent the transmission of sensation. 

2. Those which chemically destroy the fibrillse for a distance, thus 
preventing transmission of sensation. 

Remedies w t hich Benumb the Fibrillse. — Chief among tnese 
for its universality of application is dryness. Dentin, which protests 
against even the touch of an instrument while wet, has its sensitivity 
so lessened after the application of a rubber dam and drying, that it 
may be cut freely, in many cases without the aid of medicinal agents. 
So well is this recognized that isolation and drying of teeth are 
regarded as a necessary preliminary to cavity preparation. The 
degree of insensitivity induced is in proportion to the dryness. The 
drying temporarily deprives the dentinal protoplasm of a portion of 
its water, and inhibits the transmission of sensation by reducing 
functional activity. 

A continuous but gentle blast of air, passed from a compressed-air 
apparatus or double bulb through a heated metal bulb and nozzle, 
or through an electrically heated coil, should be employed until the 
dentin is desiccated. This is evidenced by its extreme whiteness. 
Other forms of hot-air syringes may be substituted with less satis- 
faction and greater fatigue to the operator. The double bulb may 
be operated by the patient. 

The application of absolute alcohol assists the drying because of 
its affinity for water. The addition of a little menthol to the alcohol 
assists by anesthetic action. The pain from the warm air may at 
first be quite severe, but even in greatly hypersensitive cases the 
nozzle of the syringe may soon be approximated to the cavity, though 
in some cases it may be necessary to make an application of a mixture 
of equal parts of carbolic acid and oil of cloves, or of gum camphor 
and carbolic acid (phenol camphor), both of which have some 
anesthetic effect. Menthol may be added to either. When desirable, 
their effect may be hastened by pressure with unvulcanized rubber. 

An instrument known as the "dehydrator" causes absolute alcohol 
placed in a special chamber between the bulb of the hot-air syringe 
and the nozzle to be vaporized upon the hypersensitive dentin. 
The drying effect is thereby augmented and the dentin satisfactorily 
obtunded. 

Some degree of dryness is, as a rule, a necessary preliminary to 
success with other applications. 

Following dryness, the excavation should be done with sharp 
instruments and burs. The latter should only be lightly touched to 
26 



402 DENTAL CARIES 

the dentin and be revolved at high speed. Letting the bur occa- 
sionally run free cools it. The heat of friction is considerable and 
highly irritating. 

The combination of potassium carbonate with glycerin makes a 
water-extracting combination having but little coagulating power. 
For this reason it may be used in the deeper cavities, but not in cases 
of almost exposed pulp, as in such cases its application is painful. 

1$ — Potassium carbonate gr. xv 

Glycerin f5j 

Mix in a mortar. 

To be applied on a pellet of cotton. (Flagg.) 

It may be used with effect even upon slightly moist dentin. 

Not being escharotic to the gum, this remedy is exceedingly useful 
about the sensitive but undecayed necks of teeth, and may be freely 
applied after moderate drying of the parts. 

If necessary, the patient may be given the prescription and directed 
to apply by means of a clean tooth-pick, which should not be used 
a second time, as the mixture may be infected and spoiled. 

Its pain simulates that of zinc chlorid, but is less severe in its 
character. 

A mixture of tannin and glycerin has a similar effect. 

1$ — Tannin 5j or 3ij 

Glycerin f3j 

Mix in a warm mortar. 

Refrigeration by a spray of ether or ethyl or methyl chlorid reduces 
the temperature of the fibrils and pulp, benumbing them. The 
rubber dam should be applied to isolate the teeth operated upon. 
Ether is applied by means of a double-bulbed atomizer, or one 
operated by compressed air; the chlorids are contained in glass 
tubes conveniently capped. The cap being raised, the heat of the 
hand causes vaporization of the agent within the tube, which forces 
the liquid out of the orifice of the tube in a fine but forcible stream. 
A spraying nozzle is also obtainable. The cavity should at first 
contain a pellet of cotton, in order that the dentin may be gradually 
obtunded and painful response on the part of the pulp avoided. The 
method may be painful in application, but often satisfactory. Ether 
odorizes the operating room, and a flame must be avoided. 

"Vapocain" and "potassocain," proprietary agents which consist 
of a 15 per cent, solution of cocain in ether, are applied to hyper- 
sensitive dentin upon the theory that the ether enters the tubules, 
carrying the cocain into contact with the fibrils; the ether evapo- 



HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 403 

rates, leaving the coram in aqueous solution to benumb them. This 
requires several minutes. They are useful in the deeper cavities. 
Jack recommends that the cavity acidity be neutralized before their 
application. 1 

Fig. 373 




Ethyl chlorid spray tube. 

A 10 to 25 per cent, solution of cocain hydrochlorate, or novocain 
in water may be forced into the tubules by applying it on a pellet of 
amadou, placing over this soft vulcanite rubber, and producing 
pressure with a burnisher for from three to six minutes. The pressure 
should be gradually applied. A gratifying degree of dentinal anes- 
thesia may often be obtained. 

Adrenalin chlorid solution, 1 to 1000, plus chloreton 2 or cocain, 
has been used in this manner with some effect. A few crystals of 
the cocain or novocain may be picked up on a pellet of cotton moist- 
ened with warm water and pressed upon the cavity surface. 

Miller 3 has shown that by taking a modelling composition impres- 
sion of the cavity, then applying a few threads of cotton saturated 
with cocain to the floor of the cavity, then placing a thickness of 
rubber dam over the entire cavity surface, replacing the modelling 
composition, and producing pressure, anesthesia can be produced 
when there is not a greasy condition of the cavity, nor thick layers of 
decalcified dentin nor much secondary dentin present. 

Cataphoresis (Greek kata, down, and phoreo, I bear or bring) is, 
in technical parlance, the transference of substances from the anodal 
or positive pole of a battery toward the cathodal or negative pole. 
They are thus carried into the tissues. 

Cataphoresis is to be distinguished from electrolysis, by which 
substances are decomposed and their elements carried from positive 
to negative or from negative to positive poles, according to their 
polarity. In cataphoresis a substance is carried unchanged from the 
positive toward the negative pole, after the manner of granules in 
protoplasm acted upon by the same force. (See p. 20.) 

1 American Text-book of Operative Dentistry. 

2 Parke, Davis & Co. 3 Dental Review, 1906. 



404 DENTAL CARIES 

As applied to dentistry, a primary current from a battery arranged 
with the cells in series has the positive pole or conductor connected 
with a resistance or current controller, capable of being so manipulated 
as to gradually reduce the resistance to the current a fraction of a 
volt at a time. This is called a "fractional volt selector." This is 
usually a broken ring of graphite, to one end of which the incoming 
current is admitted by means of the conducting cord and travelling 
indicator (from the positive or carbon pole of the battery); at the 
other end the current passes out by a similar cord, which in turn 
is attached to a milliamperemeter, or instrument recording the 
quantity of current passing through the circuit. From this a cord 
leads to the positive electrode applied to the tooth cavity. To 
the face, neck, or wrist of the patient a moist electrode (negative) 
is applied, which by its conducting cord leads the current back to 
the negative or zinc pole of the battery. The current passes through 
the patient. 

The milliamperemeter is a convenient but not an essential feature 
of the apparatus, and as a volt-selector, a rod of graphite or a glass 
tube with water resistance may be used. Fig. 374 shows the more 
elegant apparatus arranged almost as described. 

In the use of the cataphoric apparatus, the tooth is securely in- 
sulated by well-ligated rubber dam and cotton saturated with a 
solution of cocain hydrochlorate or citrate, of a strength of from 10 
per cent, to a saturated solution is placed in the cavity. The platinum 
anode is wrapped with cotton, dipped in the solution, and inserted 
into contact with the cotton in the cavity. The controller is now so 
manipulated as to gradually cut out its resistance to the current, and 
the high resistance of the dentin is gradually overcome. 

The cocain solution should be renewed as dryness occurs, as dryness 
increases the resistance. The cocain is carried along the fibrils to 
the pulp by the electric current, and dentinal, followed by pulpal 
anesthesia results. 

From eight to fifteen minutes, or sometimes longer, are required 
for dentinal anesthesia, which loss of time is largely regained in the 
facility of operation. 1 

Price 2 has shown that pulp anesthesia is gained more readily by 
concentrating the action of the cocain upon the pulpal wall by means 
of a small electrode. If general dentinal anesthesia is required he 
prefers this method, as the pain receptivity of the pulp is abolished. 
A broader application anesthetizes the dentin. 

Woodward 3 has shown that in the latter case the dentin in a cavity 

1 Jack: American Text-book of Operative Dentistry. 2 Dental Summary, April, 1903. 
3 International Dental Journal, November, 1902. 



HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 405 

upon the opposite side of a tooth being operated upon, may remain 
sensitive. 

Fig. 374 




S. S. White cataphoric outfit. 



The pulp may be anesthetized by this method for removal. In 
difficult conditions this is a very valuable means of therapeutics. 



406 



DENTAL CARIES 



The pulp is not injuriously affected in ordinary applications, unless 
saturated by long application. A reaction resulting in hyperemia may 
take place. To obviate this, the pulp should not be oversaturated, the 
fibrils should be treated with carbolic acid, and in deep cavities a 
non-conductor should be used before filling. 

In case absolute insensitivity is produced, the anatomy of the pulp 
must carefully be considered, so that it be not exposed during the 
excavation of the cavity. This can be determined by instrumental 
examination. Insulation of the pulp from thermal shock subsequent 
to filling is also to have consideration. 

The pulp may have cocain or novocain forced into it by means of 
a powerful compound-pressure syringe. The Meyers syringe is one 
of the best. It is filled with a 2 to 4 per cent, solution of cocain or 
novocain in water; a convenient drill pit is made with a No. \ bur; 
the nozzle of the filled syringe freed of air is forced into the opening 
and continuous or intermittent pressure produced without releasing 



Fig. 375 




The Meyers compound syringe for forcing cocain solutions through the dentinal 

tubules. 



the point for several minutes. It is well to allow the air to escape 
from the pit by holding loosely for a moment. No general cavity 
anesthesia will result until the solution has infiltrated the area of 
pulp underlying the fibrillar connections with the pulp. The forcing 
of cocain into so delicate a tissue should stop at that point, as more 
may produce expansive pressure, and may cause a later pulp reaction, 
as cocain is, to a degree, a protoplasmic poison. The method is useful 
in pulp extirpation rather than in hypersensitivity, but has occasional 
use, especially in cervical cavities. Secondary dentin is difficult of 
penetration, and gradual approaches must be made. It should be so 
injected into only sound dentin. If the cervix of a cavity is used as 
the point of injection, the pit should be made deeper than the syringe 
nozzle penetrates, as in this way the lateral tubules can carry the 
cocain, otherwise they may be occluded by the syringe point. The 
syringe nozzle may be made flat ended and the pit in the dentin be 
made with a cone-shaped bur. 



HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 407 

Mucous and Conductive Anesthesia. — The anesthetization 
of the branch of the fifth nerve leading from the tooth, renders it 
incapable of transmitting sensation to the brain. In principle its 
application does not differ from local application to fibrils or pulp. 
The nerve paralysis is produced nearer the brain, as it were. Novo- 
cain is at present largely substituted for cocain for this purpose. 

Guido Fischer recommends the following as an isotonic solvent: 

Calcium chlorid 0.04 gram. 

Potassium chlorid 0.02 gram. 

Sodium chlorid 0.05 gram. 

Distilled water (sterile) 100.00 grams or c.c. 

Add novocain 1.0 or 1.5 or 2.0 grams, to make a 1 to 2 per cent, 
solution as desired. At the time of use add two drops of a 1 to 1000 
solution of synthetic suprarenin to each 30 minims of solution — 
boil for sterilization. When only occasionally used, a sterile tablet 
(ready made), containing J grain of novocain and a suitable pro- 
portion of synthetic suprarenin, may be dissolved in 30 minims of 
the isotonic solvent or normal salt solution, and the whole boiled for 
sterility. A tablet (E) is made by the Farbwerke-Hoechst Company 
and consists of: 

^ — Novocain 0.02 gram. 

Suprarenin .... 0.00005 gram. 

Dissolve in 30 minims of solvent for a 1 per cent, solution and boil. 

When mucous anesthesia is employed, the solution is injected into 
and beneath the periosteum, both buccally and lingually, as nearly 
over the apex of the root as possible. About ten minutes are required 
to produce satisfactory pulp anesthesia. Fischer 1 emphasizes the 
following conditions for success in mucous anesthesia: 

1. The application of a stasis bandage slightly compressing the 
carotid artery and the veins of the neck, to help retain the anesthetic, 
and prevent cerebral anemia. 

2. The periosteum, not the submucous tissue must be infiltrated. 

3. One injection to be made on each side of the teeth. The fewer 
injections the better the effect. 

4. The part must be sterilized with tincture of iodin and the 
sterile needle must have its orifice faced toward the bone. 

5. Slow, moderately strong pressure during the injection. 

6. The point of injection must be compressed with the finger, 
after the needle is withdrawn to allow diffusion of the anesthetic. 

1 Local Anesthesia in Dentistry. 



408 DENTAL CARIES 

In conductive anesthesia, the anesthetic is injected into the tissue 
contiguous to a nerve trunk. Its infiltration causes anesthesia of 
the part it supplies. Fischer directs that for upper posterior teeth 
supplied by the posterior superior dental branch of the superior 
maxillary division of the fifth nerve, a long needle should be driven 
into the mucosa beneath the zygomatic process and then advanced 
upward and backward to the foramen at which the nerve enters the 
tuberosity of the maxilla. One c.c. of solution is introduced. Pala- 
tally a mucous injection is made at the posterior palatine foramen. 
For upper first molars an additional palatal mucous injection over 
the first molar is advised. Ten minutes is allowed for operative 
anesthesia. The upper teeth anterior to the molars being supplied 
by the infraorbital terminals their sensibility, may be blocked by 
conductive anesthesia of the nerve within the infraorbital foramen 
above the first bicuspid. A 1 per cent, solution is used. 

Fischer directs the introduction of the needle into the reflection 
of the mucous membrane just back of the cuspid apex and to be 
advanced upward and backward to the location of the infraorbital 
foramen, when some force is required to force the anesthetic into the 
foramen. Palatally a mucous injection is made parallel to the axis 
of the roots of the teeth to be anesthetized. 

For anterior anesthesia in the mandible, injection is made into the 
region of the mental foramen, and as well a lingual mucous anesthesia 
is done. For complete anesthesia of the side of the mandible, injection 
is made in the soft tissue just above the retromolar triangle in the 
inside of the ramus. Twenty minutes are allowed for complete anes- 
thesia. The technique of these injections and the local anatomy are so 
beautifully illustrated and described in Guido Fischer's book on Local 
Anesthesia in Dentistry that the reader is urged to master its details 
from a work devoted exhaustively to the subject. 1 

Diplceic Anesthesia. — For deep anesthesia about a molar, the 
gum may be anesthetized and a cut made to the bone, a small sterile 
drill is then driven through to the cancellated structure. A further 
injection is then made with a blunt needle, such as is used in high 
pressure work. This operation has been modified by the use of a 
needle constructed to simply indent the cortical layer of bone, so 
that the force of the plunger may cause the direct infiltration of the 
apical tissue. This uses the principle of high pressure anesthesia 
as applied to dentin. 

While the operation of diplceic anesthesia seems heroic, there is 
no good reason for so regarding either this or the operation of conduc- 

Theodor Blum has an excellent article in Items of Interest, for July, 1914. 



HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 409 

tive anesthesia in general as more dangerous than ordinary mueous 
injection. The rule of safety lies in knowledge of anatomy, safe 
dosage, and sterility — in short, in eorrect technique. 

The introduction of a 5 or 10 per cent, solution of cocain upon 
cotton into the nostril, upon the side of operation, is endorsed by 
Peck, of Chicago, as a means of anesthetizing the nerve trunk 
leading from the upper incisors. Escat, 1 of Toulouse, France, has 
observed that a 0.1 per cent, solution on cotton about the size of an 
almond, placed in the nostril in close proximity to the anterior edge 
of the inferior turbinate, will in twenty minutes anesthetize the 
anterior superior dental branch of the fifth nerve, which lies in close 
proximity to the nasal mucous membrane at this point. The entire 
tissue about the incisors and cuspids of the side is anesthetized, as 
is sometimes that of the opposite side in part. 

Reflex Anesthesia. — Claims are made by Dr. William H. 
Fitzgerald, M.D., that pressure with a metal probe tipped with 
cotton upon certain parts of the mouth and fingers, will produce 
satisfactory oral anesthesia and even of more distant parts. Cura- 
tive effects in certain body diseases by proper manipulation are 
claimed. The method is too new for recommendation here. 2 

Soderberg 3 has shown that painless excavation of cavities other- 
wise uncontrollable may be effected by the use of nervocidin, an 
alkaloid obtained by Dr. D. Dalma from the East Indian plant 
gasu-basu. Twenty-four hours are required for complete dentinal 
anesthesia without pulp anesthesia unless a second application be 
made. 

The primary effect of nervocidin being irritating, Soderberg recom- 
mends the additional use of cocain, both being mixed with zinc 
sulphate cement. 

1$ — Gum arabic 5J 

Zinc sulphate Bss 

Water fgj— M. 

Dissolve the zinc sulphate in the water, add the gum arabic, stir; let stand for 
twenty-four hours and strain. 

^ — Of above solution . . . f3ij 

* Nervocidin gr. x 

Cocain hydrochlorid gr. x — M. 

To a portion of the latter solution add uncalcined zinc oxid to 
make a cement, which is placed in the dried cavity. Uncalcined zinc 

1 Theodor Blum has an excellent article in Items of Interest, 1908, p. 181. 

2 Paper read before the N. J. State Dental Society, July, 1914. See Items of 
Interest to be published later, and Hogan, Items of Interest, June, 1913. 

3 Dental Cosmos, August, 1903. 



410 DENTAL CARIES 

oxid added to the first formula makes zinc sulphate cement. After 
excavation the acidity of the nervocidin should be neutralized. 
Buckley 1 has recommended: 

If — Mentholis gr. xx 

Chloroformi fgss 

Etheris f3j— M. 

Sig. — Place a little in the cavity after the rubber dam is adjusted. 

Hot water supplied by a tube leading from a coil heated by 
electricity and attached to the water supply pipe of the fountain 
cuspidor has been recommended by A. F. Merriman, Jr., for the 
obtunding of hypersensitive dentin in cases in which dryness is not 
readily obtainable, nor immediately or subsequently desirable. 

It is claimed that satisfactory analgesia is obtained, and that the 
mucous membrane of the mouth is not unduly uncomfortable, even 
when the heat is objectionable to the finger of the operator. The 
advantages of the method for excavation and grinding are obvious 
and most useful, particularly for trimming live teeth. 

Remedies which Chemically Destroy the Fibrils for a 
Distance, Preventing Transmission of Sensation. — Agents 
which chemically destroy the dentinal protoplasm form the most 
extensive group of dentinal obtundents. They include salts of 
metals, such as zinc chlorid and silver nitrate; carbolic acid and its 
derivatives, and like bodies; the cresols, etc.; mineral acids, notably 
sulphuric, chromic, and nitric; organic acids — trichloracetic and lactic 
acids — (full strength) ; alkalies — sodium and potassium hydrates and 
carbonates. 

Zinc chlorid, silver nitrate, and carbolic acid all cause coagulation 
of the fibrils of the dentin. The mineral and organic acids chemic- 
ally decompose both protoplasm and the calcified tissues. The 
concentrated alkalies chemically destroy protoplasm and bring 
about its quick dissolution. Like all active chemical substances, the 
extent of their action depends upon the freedom with which they 
are applied. 

The application of any of these agents, as a rule, causes pain, the 
degree of suffering being usually in proportion to the depth of the 
cavity. For this reason the more powerful agents, like zinc chlorid 
and nitric acid, are to be confined to cavities of moderate depth, 
while carbolic acid, especially in combination with the oil of cloves, 
may be used in the deeper ones. 

Fused zinc chlorid is used in its deliquesced form, and is most 
active when some of the salt is still undissolved in the bottle. Its 

1 Dental Cosmos, August, 1907, p. 328. 



HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 411 

pain in suitable cavities is a full, bearable one, gradually increasing, 
sometimes in waves, until a crisis is reached, when the pain gradually 
ceases. It has a double action, not only coagulating protoplasm, 
but combining with its water, owing to its affinity for the latter. 
On account of this property its action may be limited by warm water. 

An undue action of the zinc chlorid is indicated by a throbbing 
pain ; this indicates that the pulp has been irritated. When, as occa- 
sionally occurs, no pain is produced, no obtundent effect is obtained. 
If this occur regularly the drug is oversaturated with water. 

Bogue has suggested that cocain crystals be incorporated with 
the chlorid of zinc as a means of alleviating the pain incident to the 
application. 

Miller, following Hoffheinz, advocated the use of equal parts of 
zinc chlorid and chloroform. 

Buckley modified this by using the following: 

1$ — Zinc chlorid gr xx 

Chloroform, 

Alcohol aa f§ iv — M. 

Certain moderately deep cavities may be filled with oxychlorid of 
zinc cement, the free zinc chlorid acting as an obtundent. This 
requires a prolonged action, and is only resorted to in cases which 
do not admit of immediate work, or in which procrastination is 
desirable. 

A formula of wide renown is known as Robinson's remedy; this 
may be made in one of two ways: 

1$ — Potassium hydrate 

(or Sodium hydrate), 

Carbolic acid p. seq. — M. 

Reduce the gelatinous mass formed with alcohol. 

Or, 

1$ — Sodium hydrate (deliquesced), 

Calvert's crystal carbolic acid .... p. aeq.— M. (Huey.) 
The liquid formed is spoiled when it effloresces upon the sides of the bottle neck. 

The painfully caustic action of the sodium or potassium hydrate 
is modified by the carbolic acid. 

The application of Robinson's remedy is useful in the simpler 
cavities and about the undecayed but hypersensitive necks of teeth 
,and on occlusal surfaces. It is escharotic to the gum. 

If this remedy or zinc chlorid be required about the periphery of 
deep cavities the plan suggested by Jack, of varnishing the cavity 
floor with chloro-percha as an impenetrable protective is valuable. 



412 DENTAL CARIES 

A method similar to the use of Robinson's remedy consists in apply- 
ing carbolic acid to a cavity and then without removing it, placing a 
few granules of sodium dioxid. 1 Sodium dioxid alone in a slightly 
moist cavity, liberates nascent sodium hydrate (also H2O2), which 
will destroy the gum protoplasm, and is somewhat effective in hyper- 
sensitive dentin. 

Carbolic acid in concentrated form may be applied to any cavity. 
Jenkins, of Dresden, has recommended that it be used hot; it is 
particularly useful for cavities containing masses of softened dentin. 
A variation consists in the application to the cavity, upon a pellet 
of cotton, and heating it with a hot burnisher. 

Sodium bicarbonate is at times an efficacious remedy, and may be 
freely applied to the moist cavity. A 20 per cent, solution of am- 
monium carbonate, applied for five minutes or longer, is useful. 2 

The nitrate of silver powerfully coagulates fibrillar protoplasm, 
forming the albuminate of silver, which turns black upon exposure 
to the light. It is useful in posterior teeth well out of view, and to 
which the rubber dam cannot well be applied. It is also useful 
about undecayed hypersensitive necks of molar teeth. It penetrates 
the dentin for a short distance. For this reason its use is ordin- 
arily confined to posterior teeth, though in some obstinate cases of 
hypersensitive necks of lower incisors and cuspids it may be used. 
To prevent the production of hypersensitivity in teeth ground for 
bridge- work, it should be applied over the entire crown. It may be 
used in saturated aqueous solution upon the dried dentin, or the 
crystal rubbed upon the slightly moistened dentin. The crystal or 
fused silver nitrate rubbed upon abraded and sensitive occlusal 
surfaces often affords much comfort. 

Craven's method consists of taking up a few crystals upon a hot 
platinum wire, and then fusing them into a button upon its rough- 
ened end. This is then rubbed upon the dentin. 

Miller has shown that the silver deposit lessens the penetration of 
acid decalcification (Fig. 376). 

The subsequent use of sodium chlorid assists in partially removing 
the stains, argentic chlorid being formed. 

Register has suggested the use of iodin followed by ammonia for 
this purpose. 

Coming into contact with an amalgam filling, or a bit of amalgam, 
an intensely black deposit is instantly produced, which, while acid at 
first, is useful in slowly obtunding dentin in cavities out of view. 
Curiously enough, not all amalgams do this. 

1 H. J. Moore: Dental Review, 1906. 2 Thiesing: Dental Cosmos, Nov., 1903. 



HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 413 

For severe cases not yielding to local treatment at the time desired, 
the following has been recommended. 1 

1$ — Trioxymethylene 

Orthoform p. seq. 

Make into a paste with carbolic acid. 

Or, 

1$ — Menthol crystals 5 parts. 

Phenol crystals 4 parts. 

Reduce to a syrupy liquid to be used in place of the carbolic acid in the above 

formula. 

This paste is applied to the cavity walls over even decayed 
dentin, covered with a pellet of cotton, and sealed in with temporary 
stopping or cement for twenty-four hours only. Formaldehyd gas 
is liberated in the nascent state and desensitizes the fibrils by harden- 

Fig. 376 




Dentin treated with silver nitrate at a only; the entire surface subjected to acid 
action shows penetration at b. (Miller.) 

ing and fixing them as in histological specimens. The orthoform 
acts as an anesthetic during the action of formaldehyd. This prin- 
ciple has been used in cavities with the ordinary 37 per cent, 
formaldehyd solution, applied by the pressure method, and is useful 
about the hypersensitive necks of teeth. Buckley 2 has recently 
introduced a modification in a paste form having similar action. 

1$ — Xeothesin (Lilly) 3^o grain. 

Trioxymethelene ^3 grain. 

Thymol 2T0 grain. 

Petroleum base, coloring matter, and fibre. 

(The figures indicate the approximate quantities in one application.) 
S. — Apply to dry dentin and cover with cement for twenty-four to forty- 
eight hours. 

1 G. Mahe, M.D., Paris: Dental Cosmos, 1904. 

2 Items of Interest, December, 1914. 



414 DENTAL CARIES 

In shallow labial cavities it is to be applied and covered with 
very adhesive cement. 

In shallow cavities and upon abraded surfaces, nitric and chromic 
acid accurately applied in small quantity upon a gold probe is 
useful. Any softened dentin must later be removed and filled. 

For very obstinate cases of cervical hypersensitivity, Flagg recom- 
mended the use of the electric cautery, the spots to be seared. A 
very hot burnisher may occasionally serve. 

Aside from the treatment of hypersensitive dentin, at the time of 
operation, analgesics may be introduced for their power of gradu- 
ally lessening the hyperirritability of fibrillar protoplasm. If cotton 
wedges are introduced, antiseptic analgesics, particularly oil of 
cloves (or eugenol), equal parts of oil of cloves and carbolic acid, 
and phenol camphor, or Fletcher's carbolized resin, may be used on 
the cotton with advantage. 

A partially prepared cavity may be moistened with eucalyptol 
and temporarily filled with temporary stopping or gutta-percha. 
This affords rest. If the gutta-percha leak, the cavity will be more 
sensitive. 

A temporary filling made by mixing zinc oxid with Fletcher's 
carbolized resin or eugenol to a stiff paste will endure for some 
time, and reduce hypersensitivity. It is also useful as an antiseptic 
sedative test filling. 

1$ — Carbolic acid, 

Colophony aa §j 

Chloroform fgss — M. 

(Fletcher.) 

The use of chalk applied nightly in a superficial cavity, as at the 
cervix, is useful for this purpose. 

In cases in which devitalization is intended, arsenic may be used 
as an obtundent to effect a deeper placing of another portion as a 
devitalizing agent; twenty-four to forty-eight hours are required for 
this purpose. If left long enough it will devitalize the pulp even 
through a large mass of dentin. 

There is no safety in short applications as a means of obtunding 
dentinal hypersensitivity. The pulp may die even after seeming 
excavation of all affected dentin. 

Ninety per cent, of cavities may be comfortably excavated with 
sharp instruments by the aid of dryness and carbolic acid or simple 
obtundents. A small percentage require the use of strong caustics, 
etc., while in a still smaller number some of the extreme measures 
are necessary, though nitrous oxide is admissible in all cases. 



HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 415 

During seasons in which acid fruits arc consumed, much hyper- 
sensitivity may be induced. This should always lead to examination 
for cavities of decay, but such may not exist or may be properly 
filled. 

For hypersensitivity about undecayed necks of teeth, the mouth 
should be kept in an alkaline condition by means of dilute phenol 
sodique or sodium bicarbonate, or, better, by the use of more lasting 
mild alkalies, such as chalk, or milk of magnesia, or a combination 
of the two. The manufacturers of milk of magnesia recommend a 
series of oil mixtures; 6 drops of any mixture to be shaken up with 
the contents of the original bottle as a flavor to remove the naturally 
raw taste of the preparation, which is disagreeable to some persons. 1 
The following are two of the simplest. 

~ty — Oil of bitter almond 1 part. 

Oil of anise 3 parts. 

Or, 

1$ — Oil of cinnamon 3 parts. 

Oil of wintergreen 4 parts. 

The use of potassium carbonate in glycerin is indicated and may 
be given to the patient for free use. 

For hypersensitive incisal edges or occlusal surfaces, Robinson's 
remedy may be thus dispensed with a caution as to its caustic nature. 

At times zinc chlorid, Robinson's remedy, and silver nitrate or the 
actual or electric cautery must be used by the operator. 

In a number of the localized cases fillings may be subsequently 
required unless rigid prophylaxis be practised. Prophylaxis may 
remove the superficial desensitized layer, and the application require 
renewal. I have been informed that a case of general hypersensiti- 
vity was cured by the lemon juice treatment given for systemic con- 
dition. The idea is worthy of attention. It might be explained 
upon the principle of induced alkalinity of salivary secretion as 
organic acids are known to increase the alkalinity of the urine. 

In cavities not permitting exact excavation, oxyphosphate of 
copper cement left for a considerable time will often reduce exquisite 
sensitivity. 

The use of potassium sulphocyanate internally in case of great 
general dental hypersensitivity has had good results claimed for it, 
especially in pregnant women. (See p. 361.) 

1 Items of Interest, 1905, p. 977. 



CHAPTER XIV. 

DENTAL CARIES: THERAPEUTICS AND PROPHYLAXIS. 

According to the depth of invasion and variations in the thera- 
peutics involved, caries may be divided into eight stages, as follows: 

1. Superficial caries, or that stage in which the enamel has been 
partially decalcified, but the dentin not affected (Fig. 338). 

2. Simple caries, in which the dentin has been affected slightly, 
in such manner as ordinarily to compel the formation of a cavity 
and its filling (Figs. 344 and 347). 

3. Deep-seated caries, in which the complete excavation of the 
cavity renders pulp injury a possibility, but the pulp is not very 
dangerously approached (Fig. 353). 

4. Almost exposed pulp. This is a refinement of the preceding 
stage, in which pulp exposure becomes imminent during excavation 
of the cavity and special therapeutics are demanded (Fig. 377). 

5. Exposed pulp, in which the actual exposure of the pulp by 
decay or by accident or intention during excavation renders its 
treatment necessary, or in which disease of the pulp compels canal 
treatment. 

6. Perforation by caries, in which after pulp death secondary caries 
of dentin and cementum has caused an opening into the pericemental 
tract (an extension from the condition in Fig. 362). (See Fig. 378.) 

7. Loss of crown by caries. 

8. Loss of root by caries. 

Each of these stages of caries requires special consideration and a 
therapeutics adapted to each. 

THERAPEUTICS OF SUPERFICIAL CARIES. 

About cavity margins, beneath green stain, etc., along bucco- 
cervical margins, and at points of approximal contact of teeth may 
frequently be seen areas of enamel decalcification, the enamel not 
being entirely penetrated (Fig. 338). 

It is possible at times to remove the decalcified portion by means 
of carborundum strips, files, or disks. If the surface be highly 
polished by means of pumice and chalk, and subsequent prophyl- 
axis be employed, the practice may be endorsed for the better grades 
(416) 



THERAPEUTICS OF SIMPLE CARIES 417 

of teeth, and particularly in the anterior part of the mouth. As a 
rule, however, the attempt to remove supposed superficial enamel 
caries demonstrates the fact that the enamel is deeply affected, and 
in all probability the dentin as well. The attempt to remove such 
caries upon proximal surfaces by files and stones results in tooth 
deformity, the exposure of dentin to the fluids of the mouth, and the 
destruction of the contact points, except, perhaps, when in the 
anterior teeth a lingual approach is made. It is sometimes proper to 
remove the slight superficial caries found about a cavity, either prior 
to excavation in order to determine the real cavity boundary, or 
after excavation if such removal would give an even better tooth 
form, and lessen a recurrence of decay, or, in some cases, after filling 
when both filling and margin are reduced together to a proper 
form and integrity of enamel. Some judgment is required in such 
a matter, and no enamel should be so treated if any doubt exist as 
to its future integrity, but the cavity should rather be extended to 
include the doubtful area. 

It may be considered a safe rule to examine, by means of the electric 
mouth lamp, any cases of suspected superficial caries in order to 
determine the depth of enamel invasion. 

The large majority of such cases, especially in the poorer grades 
of teeth, will be found to be of the class called here simple caries. 

Upon the labial or buccal surfaces of anterior teeth a superficial 
decalcification may be found. Whether (1) this shall be removed 
and the surface polished, or (2) be left for the patient to care for 
by exact prophylaxis, or (3) be excavated and filled, depends upon 
the location, the depth of penetration, and the progress of the 
enamel decalcification. The writer has carried forward for a long 
time numerous white crescentic markings by prophylaxis which 
removes microbic plaques .and food and aborts decalcification, 
though not removing the tissue decalcified. 

In posterior teeth staining with silver nitrate alone or by touching 
later with amalgam to produce a rapid deposit of silver, grinding 
off with stones and then touching with silver nitrate, or filling the 
actual cavity with oxyphosphate of copper and staining and watch- 
ing the remaining decalcification, have all given good results when 
conjoined with improved prophylaxis by the patient. Superficially 
decayed cementum may be removed or not and silver nitrate applied. 

THERAPEUTICS OF SIMPLE CARIES. 

The cases cited above as requiring excavation and all detectable 
cavities of very limited depth may be classed as cases of simple 
caries. . The teeth should be wedged apart if this be needed for access, 

27 



41S DENTAL CARIES 

all decalcified enamel and dentin removed, the cavity properly 
extended and shaped, and, as a rule, a metal filling inserted. All 
fissures about a cavity should be freely opened to their extremities, 
and made a part of the general cavity. 

The extension upon approximal surfaces should include all super- 
ficial decay that cannot be so disked off as to bring the filling margin 
into the embrasures. 

The treatment of simple approximal cavities is a difficult question. 
Undoubtedly extension enhances the longevity of. the fillings. At 
times, however, the cavities may be kept purely approximal and by 
the use of gutta-percha, silicate cement or combination of amalgam 
and cement renewed or repaired as required, the case can be con- 
trolled for many years. This may be advisable in anterior teeth 
where gold may be objectionable or when systemic conditions or 
uncontrollable sensitivity warrant it. In the main, if endurable, 
cavities in posterior teeth should be extended, otherwise the renewal 
of the fillings will probably in time be necessary. In the anterior 
teeth esthetics often warrants keeping the cavities small. The 
question is one which can be settled after consideration of all the 
requirements. Subsequent prophylaxis is of importance, and to that 
end all fillings should be made as smooth and perfect as possible. 

If a simple cavity prove inordinately sensitive, the more powerful 
remedies may be freely used to reduce the hypersensitivity, and the 
cavity should be treated with carbolic acid before filling, particularly 
when gold is to be used in cervicolabial cavities of incisors. By this 
means the subsequent effect of thermal changes is lessened. 

THERAPEUTICS OF DEEP-SEATED CARIES. 

In this stage of caries there is usually, although by no means always, 
an easily discoverable cavity of size (Fig. 353). After the removal 
of ragged and overhanging enamel margins, and of loose debris in 
the cavity, it is noted that the response to thermal impulse is painful 
and prompt. In washing such cavities, water at a temperature of 
about 100° F. should always be used; cold or very hot water being 
only employed in cavity irrigation to test the promptitude of response 
upon the part of the pulp. It is better to do this habitually. 

In treating hypersensitivity of dentin carbolic acid is to be pre- 
ferred, the mineral acids are avoided, and if strong agents like zinc 
chlorid or Robinson's remedy are used, the cavity floor is to be 
varnished with chloro-percha or "cavitine" varnish, which are 
impermeable. If necessary the sedative temporary methods may 
be employed. (See p. 414.) 



THERAPEUTICS OF DEEP-SEATED CARIES 419 

The use of nervocidine or of trixymethylene are most applicable if 
sittings are a few days apart. For methods of dealing with hyper- 
sensitivity see p. 393. 

Cocain cataphoresis is regarded as admissible in all stages of caries. 

The removal of all the softened dentin, which should be done in 
these cases, forms a cavity of such magnitude that proximity to the 
pulp is evident. The softening has proceeded for a distance beneath 
the enamel, so that when all softened dentin is cut away from beneath 
it the latter tissue may overhang the general cavity unsupported. 
These overhanging walls are cut away until the region of strong 
enamel is reached, and then it may be that the walls still overhang 
the general cavity. It is usually not necessary nor advisable to 
remove this portion of enamel. 

At the completion of excavation the pulpal wall of the cavity will 
be in fair proximity to the pulp. A blast of cool air from a chip 
syringe may produce an immediate response upon the part of the 
pulp, vigorous in proportion to the thinness of its dentinal covering 
and its irritability. 

In many cases non-conducting substances are required as inter- 
mediates between the pulpal wall and the metal filling. In many 
other cases the metal filling may be placed directly upon the dentin 
without danger. In some cases a simple layer of non-conducting 
varnish, such as " cavitine," 1 will be sufficient. In others zinc phos- 
phate or gutta-percha must be added. The degree of the response to 
a blast of cool air will afford a guide to the nature of the intermediate 
required if any be deemed necessary. In no case should varnish or 
gutta-percha be allowed to remain in the portions of cavity that 
support the covering filling material, and which is subjected to the 
force of mastication. The resilient nature of such substances will 
cause the loosening of the filling and probably induce mechanical 
or infective irritation of the fibrils and through them of the pulp 
(Fig. 377). 

In some cases the undermined state of the enamel wall necessitates 
the use of an adhesive zinc phosphate as a means of support by 
replacing the lost dentin, and in such the pulpal wall may be covered 
and so protected from impact as well as from thermal changes. 

The action of zinc phosphate upon dentinal fibrils and the pulp 
being a matter of some doubt, it is better that the pulpal wall be 
varnished before it is introduced. The varnish not only acts as an 

1 Cavitine is a solution of trinitrocellulose in subacetate of amyl. Gum sandarac in 
alcohol, gum copal in ether, or Canada balsam or gum dammar in chloroform, about 
30 to 60 grains to the ounce of solvent and a little hydronaphthol added, makes an 
antiseptic cavity varnish. 



420 



DENTAL CARIES 



Fig. 377 




impervious coating, but also serves as an additional non-conductor. 
If made antiseptic it is still more useful. 

After the cavity is prepared it is sterilized and dried, as described 
in the next stage of caries, is coated with varnish, and Harvard zinc 
phosphate plus 5 per cent, powdered thymol 
mixed stiff is packed into the undercuts and 
over the pulpal wall, and approximately formed. 
When set the enamel margins are freed of 
cement and the cement is excavated to the form 
required. In some cases cement can only be 
placed over the pulpal wall, owing to lack of 
room for both cement and the covering filling. 
In such cases the combined use of soft cement 
and gold, or soft cement and amalgam, is useful. 
In deep-seated caries the extension of cavity 
margins in such a manner as to prevent re- 
currence of decay is demanded. Upon approxi- 
mal surfaces the ideal conditions are an extension 
of buccal and lingual margins to a point which 
will permit a contoured metal filling to have 
its corresponding buccal and lingual margins 
well irrigated by the action of the tooth-brush 
and food in mastication. Often a slight alter- 
ation of tooth form, together with contouring 
of fillings, accomplishes the end desired without 
undue cutting of tooth structure. Thus the 
cervical margin may be slightly reduced with strips or disks to assume 
an absence of contact, but the enamel must not be totally removed. 
The lingual or buccal margin may be treated in a similar manner. 

The cervical margin of the cavity and filling are best protected 
when overlapped by healthy gum tissue, and if the gum be ap- 
proached, should be so arranged. The cervical margin should always 
be extended beyond the contact point in such cases, whether carried 
beneath the gum or not. Incisal margins are to have similar con- 
sideration. 

Firm approximal contact of fillings or filling and tooth are required 
to prevent packing of food into the interproximal space. This would 
both injure the gum and introduce the fermentable element in caries 
production. The point of contact should be neatly rounded to 
produce a normal contact. This contact should be obtained even if 
the filling must be overcontoured. 

An exception may at times be made where a space has previously 
naturally existed, and the gum margin is healthy. 



Diagram illustrat- 
ing the use of pulp 
protectors: V, a 

layer of varnish; GP, 
a layer of low heat 
gutta-percha, or in 
case of exposure a 
layer of Jodoformagen, 
or zinc oxid and thy- 
mol in which case the 
varnish is omitted ; 
ZP, zinc phosphate; 
with or without thy- 
mol added; M, metal 
covering. 



THERAPEUTICS OF ALMOST EXPOSED PULP 421 

Teeth should never be joined by fillings alone, as one or both will 
usually loosen. If necessary for the protection of the gum, both may 
be crowned and the crowns united by solder, or a staple may be 
placed in the pulp canals of the two teeth. About this a common 
filling may be built. It may be that gold inlays, locked in spacious 
"doll heads" or the occlusal surfaces of both teeth, and extending 
over to distal approximal surfaces as well as into the cavities, may be 
joined or cast double as a means of support. The strain upon such 
fillings is very great when occlusion exists, as teeth are bodies with 
individual motion and are apt to be pushed away from the filling. 
(See Pyorrhea Alveolaris and Gingivitis.) 

THERAPEUTICS OF ALMOST EXPOSED PULP. 

In this stage of caries complaint is usually made that for some 
time pain has been produced by the presence in the mouth of cool 
or hot substances. Several classes of almost exposed pulps may be 
discovered after opening the cavity and removing the bulk of the 
decayed dentin. In the simplest class the pulpal wall may be found 
sound after removal of all decalcified dentin. This makes practically 
a case of deep-seated caries, and is to be treated as such, the close 
approach to the pulp simply demanding additional precautions as 
to non-conduction, prevention of compression, and infection. The 
cavity is to be neutralized with a solution of sodium bicarbonate or 
5 per cent, sodium dioxid solution, etc., and dried; over the pulpal 
wall "cavitin" with hydronaphthol added or other antiseptic varnish, 
and dried again. 

1$ — Hydronaphthol gr. ij 

Alcohol gtt. xx — M. 

Add to the half-ounce bottle of "cavitine." 

A thin wafer of softened gutta-percha is to be laid over the pulpal 
wall in such manner as not to interfere with the introduction of 
cement. In place of these any of the pulp capping cements may be 
used as a first layer (Fig. 377). Harvard zinc phosphate mixed to 
consistency just suited to the case may be pressed laterally into the 
undercuts, and will spread nicely over the gutta-percha without 
pressure. Under no circumstances must the superstructures depend 
upon the gutta-percha base as a support, as the filling may loosen 
or the wall be broken. 

The operation may be varied for cases of but limited retaining 
periphery by gently spreading the zinc phosphate over the varnish, 
or, in some cases, the gold and zinc phosphate or amalgam and zinc 
phosphate combination may be required. 



422 DENTAL CARIES 

In the use of gold and zinc phosphate a portion of crystal gold is 
gently tapped into a mass of soft, quick-setting cement placed over 
the varnish and the setting of the cement awaited. The gold is then 
condensed and more added. 

With the amalgam and zinc phosphate combination, after placing 
the gutta-percha, soft cement is placed upon one cavity margin, 
and a ball of previously prepared amalgam is laid upon it. Pressure 
upon the amalgam by means of a ball burnisher causes the cement to 
be spread over the cavity wall in advance of the amalgam. It practi- 
cally inlays the metal filling, but permits a better marginal joint with 
the metal. The margins are freed of amalgam and cement, and the 
operation is completed with amalgam. It also prevents the shifting 
and dislodgement in any degree of the metal filling which sometimes 
occurs in the act of introduction, unless guarded against. 

This, of course, refers to locations in which the latter is indicated. 
The cement in the combination increases the adhesion and prevents 
leakage and the discoloration of the walls by the amalgam. A trifle 
of thymol added to the cement (1 to 20) imparts to it an antiseptic 
character without impairing its integrity as a cement. 

The second class of almost exposed pulp is that in which thorough 
excavation would cause exposure of the pulp. 

If the dentin be of the disintegrated, boggy sort, it should be 
removed regardless of exposure; but if it be simply softened by 
decalcification and be quite firmly adherent to the cavity floor, and 
particuarly if it be somewhat thickly distributed, the deeper layers 
may be left in situ, as a pulp covering. 

In such cases all lateral walls should be thoroughly excavated and 
only a thin layer left over the pulp horns. While, without doubt, the 
tubules of decalcified dentin are liable to be invaded by bacteria, 
Miller has shown that frequently such dentin may exist without 
invasion. (See Fig. 356.) 

The argument that such dentin contains poisonous products of 
bacteria deleterious to the pulp does not seem borne out by results 
in carefully handled cases. Decalcification is not putrefaction. 

That some of these protected pulps may die is a fact not to be 
disputed, but that many live in security is also true. Whether such 
dentin can be recalcified has not yet been scientifically shown, but 
certain cases treated with oxychlorid of zinc have shown evidences 
of it, and Miller records cases of hardening of such caries even 
without treatment. 

The treatment required for this dentin is: (1) Neutralization of 
the acid present; (2) saturation with a permanent antiseptic; (3) an 
antiseptic non-conductive covering. 



THERAPEUTICS OF ALMOST EXPOSED PULP 423 

After drying, a weak solution of sodium bicarbonate or ammonium 
carbonate will accomplish the first requirements. The dentin is then 
thoroughly dried and saturated with "cavitine" varnish containing 
hydronaphthol, or a solution of Canada balsam containing hydro- 
naphthol, or thin chloro-percha containing aristol or iodoform, or 
the formaldehyd preparation known as " Jodoformagen" may be 
spread over it, or oxychlorid of zinc, the fluid of which has been 
diluted one-third with water, may be used as a covering (use fluid, 
2 drops; distilled water, 1 drop), or a mixture of zinc oxid and thymol 
may be melted over it. 

Williams 1 suggests that the decalcified dentin be first saturated 
with absolute alcohol for one minute, then dried, then wet with oil 
of cloves for one minute, then again dried, after which the varnish, 
etc., is to be used. Solution of sulphate of copper may be used to 
saturate the dentin, after which it should be dried and encased in 
varnish, etc. This last only in posterior teeth. 

The use of these preparations obviates the necessity of sealing 
temporary antiseptics in the cavity, as they are in themselves more 
or less permanently antiseptic. The rigid preparations are most 
convenient. Over them zinc phosphate, made antiseptic with 
thymol (1 to 20), is packed or flowed, and if any doubt exist, the 
cavity is temporarily sealed with gutta-percha or temporary cement. 
When all doubt is at rest the metal filling may be placed. In another 
method, useful in doubtful cases in determining the possible bad 
reaction of the pulp, a quite stiffly mixed paste of eugenol and 
Hubbuck's zinc oxid may be introduced into the base of the cavity, 
gently pressed to place with cotton, and covered with sandarac on 
cotton, or at a subsequent sitting part of it may be left as a reason- 
ably firm antiseptic foundation. If desired, the entire cavity may 
be filled with it, or better, to a slightly concave surface. Exposed 
to the saliva it hardens to a degree sufficient to act as a cement 
temporary filling for weeks or months, or, occasionally, even years. 2 

In some cases of deep-seated caries in which gold filling is desirable, 
but in which linings are contra-indicated, yet in which immediate 
filling with metal would involve such thorough excavation as to 
endanger pulp vitality either as the result of excavation or subsequent 
thermal shocks, oxychlorid of zinc may be placed in the peripherally 
prepared cavities, and over considerable masses of decalcified dentin. 
If allowed to remain for several months (three to six) the oxychlorid 
stimulates the pulp to the formation of some secondary dentin, and 
complete excavation to a sound basis may be made. There is also 

1 Items of Interest, 1898. 2 Dr. S. Blair Luckie. 



424 DENTAL CARIES 

some evidence of hardening of the dentin. This method is open to 
the possible objection that secondary dentin is a source of future 
trouble, but the method has its advantages in badly decayed anterior 
teeth. 1 In very deep cavities the fluid of the oxychlorid should be 
diluted one-third with distilled water for the first portion. 

In these cases porcelain inlays, with their underlying cement, 
should have due consideration as therapeutic means. 

In deep and very deep-seated caries, in situations in which dis- 
coloration is not of great moment. Jodoformagen may be placed 
over the pulpal wall, avoiding the bearings and the cavity filled with 
oxyphosphate of copper for its antiseptic value. The cavity may be 
entirely filled with it, or it may be used as a combination with 
amalgam. Copper amalgam alone ordinarily becomes disintegrated 
and caries recurs. Occasionally it lasts well (especially Sullivan's); 
copper and its salts are germicidal in a short time. The ordinarily 
good behavior of somewhat doubtful dentin under it is thus explained. 

Dobrzyniecki 2 (Budapest), in eight experimental cases upon 
microscopically sound-looking dentin, claims to have found the 
Bacillus gangrense pulpse vital after months of enclosure under 
sealed dressings of camphor, concentrated Carbolic acid, or eucalyp- 
tus oil. All other organisms were devitalized. As Arkovy's 3 experi- 
ments showed the decided influence of carbolic acid over this 
organism, and as root-canal antiseptics are nearly always successful 
in cases of moist gangrene of the pulp (Bacillus gangrense pulpse 
Arkovy), the difficulty of destroying this germ by germicides left 
indefinitely in the cavity must be accepted with reservation. 

In some desperate cases with the walls frail, the cements, either 
zinc phosphate or so-called silicate cements, or oxyphosphate of 
copper cements, may be used as a last resort before crowning. The 
silicate cements are less soluble in the acids contained in saliva or 
formed from carbohydrates against the filling than are the zinc 
phosphates. 

Hinkins and Acree 4 claim that one-fifth of 1 per cent, is sufficient 
to dissolve the zinc phosphate, and that enough acid elements enter 
from the blood to affect it. 

The silicate cements dissolve more readily under friction than 
under the action of acid, so that of two fillings the one which is not 

1 In some cases of this sort seen by the writer, and observed for from ten to twenty 
years, the ill-results of oxychlorid of zinc claimed have not been observed. In one case, 
after sixteen years, a lateral incisor crown broke off, and the pulp was found to have 
receded, but was otherwise apparently healthy. The question is one of the advisability 
of immediate devitalization, with its advantages and disadvantages in anterior teeth, 
or of a possible remote pulp death, etc. 

2 Soderberg upon Arkovy: Dental Cosmos, 1899. 3 Ibid. 
4 See Dental Cosmos, June, 1901, and March. 1905. 



THERAPEUTICS OF EXPOSED PULP 425 

exposed to attrition or brush action is usually in better condition 
after about two years. Much care is necessary to prevent the dis- 
coloration of silicate cements. 



THERAPEUTICS OF EXPOSED PULP. 

The exposure of the pulp may be the direct result of caries; the 
removal of boggy, disintegrated dentin may produce it, or it may 
be the result of the removal of a last layer of decalcified dentin 
or of the careless or inadvertent perforation of sound dentin by 
instruments. Fracture or abrasion are occasionally responsible for 
exposure. Erosion rarely causes it. 

Diagnosis. — After excavation of the cavity, washing w T ith tepid 
water, and moderate drying, direct vision or a reflected image in the 
mouth mirror may reveal the area of exposure as a round opening 
occupied by a pinkish or red body. If the exposure be reasonably 
large, pulsation of the red body may usually be observed. The 
exposure may be so slight as to be invisible, the depth of the cavity, 
however, indicating that exposure probably exists. Bleeding is a 
certain guide, but bleeding from the gum margin must be borne in 
mind. Truman advises that finely carded cotton be gently passed 
over the cavity walls, exposure being detected by the momentary 
pain produced when the fibres pass over the area of exposure. 

As this test may fail, in cases of known exposure, it is not altogether 
reliable, but is fairly so when pain is produced, though hypersensitive 
dentin must be borne in mind. 

A finely pointed probe may be gently dragged over the pulpal 
wall and catches in the orifice of exposure, however small. A slight, 
quick start upon the part of the patient is usually elicited. This may 
consist simply of a winking of the eyelid. Flagg warned against 
requesting an affirmative nod by the patient, as this would cause 
injury to the pulp. Delicately used, this test is the most reliable in 
all classes of cases, and is not painful. 

It is to be remembered that disease may have caused a loss of a 
portion of a pulp horn, in which case the cotton test will fail; gentle 
exploration will detect the amount lost. Blood, or pus followed by 
blood, or sensation after entering the horn of the pulp cavity, are 
evidences of exposure. 

Excruciating pain following mastication, or pressure or suction 
exerted upon the cavity by means of the tongue, are subjective symp- 
toms indicating a probable diagnosis of exposure. Increase of pain, 
or throbbing pain following the use of salt, sweet, or acid foods, is 
fairly indicative of a practical exposure. 



426 DENTAL CARIES 

Treatment. — An exposed pulp is either to be capped or removed 
and the canals filled. 

The consensus of opinion is that ordinarily all pulps should be 
removed, except those freshly exposed by removal of simply decal- 
cified dentin and by accident. There is no certainty that pulps 
exposed by caries or practically so will live under capping materials, 
but the attempt may be made at times for special reasons. 

Freshly exposed pulps may be capped or removed. Perhaps a good 
rule would confine capping to anterior teeth of the better grades in 
patients in good physical condition, and to pulps in teeth having 
incomplete roots. The improved methods of pulp removal and canal 
antisepsis warrant pulp destruction as a safer method than capping 
in most posterior teeth. Even in anterior teeth pulp removal for 
anchorage purposes, if needed, is quite warrantable. The advan- 
tages of capping are maintenance of tooth translucency and the 
avoidance of canal work. 

The disadvantages are: (1) Possible death of the pulp by hyper- 
emia due to conduction of thermal changes. (2) An overproduction 
of secondary dentin, the production of pulp nodules, or other degen- 
erative changes, the pulp becoming exhausted and death ensuing. 
Increased difficulty of canal treatment may result. (3) Disease of 
the pulp due to infection beneath the capping material. (4) The 
time required for assurance of success or failure. 

The object sought in capping is the protection of the pulp from 
thermal changes, infection, and compression, as either is fatal to pulp 
vitality. This is best accomplished by placing in contact with the 
pulp an antiseptic paste beneath a metal cap, or an antiseptic 
cement having, when set, sufficient rigidity to permit other work 
to be done. In the latter case the capping material may be spread 
over the pulp by means of an instrument or be carried on oiled paper 
which may be stripped off after the cement has set. 

Prognosis is favorable for the cases selected as suggested. 

Pulp Capping. — The metal cap should be made of platinum or gold 
for anterior teeth. Tin, lead, or silver may be used posteriorly. After 
punching or trimming to shape it should be made concavo-convex 
by pressing it into soft wood by means of the rounded end of an 
instrument handle. A film of wax is placed on the convex side; 
a warmed, small burnisher is attached, and the cap is adjusted in 
proper position by trying in the cavity. It is then to be filled with 
the capping material (a little of the latter placed in any depression 
at the point of exposure in order to exclude air) ; then one side of the 
cap is laid upon the dentin and the other gradually brought down, 
and the edges of the cap firmly adapted to the dentin. This causes 



THERAPEUTICS OF EXPOSED PULP 427 

the paste to exude from beneath the eap. Any excess is gently 
removed with an excavator if not of an immediately setting paste. 
A little soft, quick-setting, zinc phosphate cement plus thymol or 
oxychlorid of zinc cement is now run over the floor as a protection 
and when set is allowed to go as a test. Later a partial excavation 
of the cement is done and better zinc phosphate or silicate cement 
placed, or gutta-percha used as a further test, which is allowed to 
remain a year. 

These may be renewed as worn out if desirable, or a portion of 
the covering filling may be cut away and metal introduced. In all 
cases capping materials are not to be allowed to support the super- 
jacent filling materials which should have their own support upon 
the cavity walls as shown in Fig. 377). In case a plastic filling is 
desirable in any event, the operation is to be completed at the time 
of capping or at a subsequent sitting. 

The materials used with success as pulp cappers are: 

1. A mixture of oil of cloves and zinc oxid (equal parts of car- 
bolic acid and oil of cloves may be used as the menstruum). Hub- 
buck's zinc oxid or cement powder may be used. This is mixed to a 
consistency which will flow, yet set after some hours or days. 

2. Oxy sulphate of zinc, the fluid of which is a saturated solution 
of zinc sulphate in water. The powder is uncalcined zinc oxid. This 
will make a thin, creamy paste which flows readily and sets quickly. 
A trifle of aristol, iodoform, or hydronaphthol may be added to any 
setting cement. 

3. Plaster of Paris mixed with a 1 per cent, solution of formaldehyd 
in water will make an antiseptic, quick-setting paste. 

4. " Jodoformagen." This substance is said to have a mixture of 
eugenol and carbolic acid for the fluid, while the powder is of zinc 
oxid, containing paraform, the solid form of formaldehyd. It also 
contains salts of iodin. A cement is formed which sets quickly, 
and must, therefore, be made very thin when placed in the cap. 
This material has been successful as a capper even in exposures by 
caries, owing to its intense germicidal power. It is claimed that 
the formaldehyd penetrates the tissue of the pulp for a distance, 
yet permits its return to normality. 

5. Oxychlorid of zinc, with the fluid diluted with 50 per cent, of 
distilled water (1 to 2), will cap successfully. It is well to add a little 
powdered thymol to lessen irritation and add antisepsis. 

.6. Crystallized thymol can be gently melted on the end of a 
burnisher and dropped on the point of exposure to crystallize, or 
a piece of a mixture of thymol and zinc oxid, made by melting the 
former and incorporating the latter, may be added to the drop of 



428 DENTAL CARIES 

thymol in position and melted with a warm burnisher. Setting 
cappers may be used without metal. Of these capping materials 
the writer prefers jodoformagen, which though proprietary, has posi- 
tive sedative as well as germicidal and persistent antiseptic value. 

Results of Capping. — If pain be initiated when the cap is placed 
and recur later, compression has occurred, and the capping must be 
removed, the pulp quieted, and the capping renewed or the pulp 
removed. Though no sensation be produced at the time of operation, 
a reaction to thermal changes may occur. If this gradually subside 
as counter-irritants are used, a diagnosis of arterial hyperemia (aseptic) 
is confirmed. If the reaction increase, the heat become more irri- 
tating than cold, and if at the same time paroxysms of pain or reflex 
pain occur, the diagnosis is that of venous hyperemia or infective 
inflammation, according to the character of the symptoms, and the 
pulp must be removed. In cases of incomplete roots the large fora- 
men prevents the formation of a venous stasis. Even if the pulp be 
kept alive only until root completion, much good will be done. As an 
example, in one case a lower second molar, exposed by caries and 
capped at the age of fourteen, at twenty-five years reacts as vital 
to an interrupted electric current, and is perfectly comfortable. 

A pulp may remain quiescent for weeks or months and then un- 
favorable symptoms set in, or it may die without any apparent pain. 
It is probable that in the latter case some reflex pains have been felt, 
but not related with the tooth, in the mind of the patient. 

In the successful cases, either the orifice of exposure is covered 
over by a deposit of secondary dentin, or the pulp remains perfectly 
quiescent beneath the capping material, without formation of deposit. 

Even when a deposit occurs the pulp may die from the atrophy 
and degeneration attendant upon the formation of much secondary 
dentin, and when no deposit occurs infection following leakages 
about filling and capping materials may take place after years of 
apparent success. While capping may be, and has been, successful 
in all grades of exposure, there is no certainty of success in the 
exposure by caries. The tentative treatment necessary offsets the 
labor of canal treatment. The alternative to capping the pulp is 
its removal. This requires a special chapter (which see). 

THERAPEUTICS OF PERFORATION BY CARIES. 

The progress of secondary caries in the dentin about the pulp 
chamber hollows out the root until at least at one point the chamber 
wall is but a decalcified layer of cementum covered by decomposing 
dentin. At some point the pericemental tissue will be uncovered by 



THERAPEUTICS OF PERFORATION BY CARIES 



429 



excavation or by the carious process (Fig. 378). The crown will 
probably be badly decayed. Taking, as an example, a lower molar 
perforated at the bifurcation with the pericemental tissue hyper- 
trophied into the opening (fungous gum), its treatment may be 
described as follows: The gum is first to be pressed out with cotton 



Fig. 378 



Fig. 379 





Diagram of treatment of perforation 
by decay. 



Crowning of divided roots. (Evans.) 



medicated with an antiseptic varnish. Fletcher's carbolized resin, 
or aristol in chloroform, or sandarac varnish plus orthoform, will 
serve. 

If immediate work be desired, polypoid fungous gum may be 
saturated with trichloracetic acid and cut away without bloodletting 



Fig. 380 



Fig. 381 




Cantilever crown. (Evans. 1 ) 




Diagram of a lateral perforation treated with 
gutta-percha; successful for seven years, when 
breakage of the crown occurred including the 
perforation: GP, gutta-percha; OZ, oxychlorid 
of zinc; A, amalgam. 



by means of a large, sharp, spoon excavator, or cocain or ethyl 
chlorid may be used for local anesthesia. Large, rose-head burs are 
used to free the cavity of all decay. The canals are opened and 



1 Artificial Crown and bridge-work. 



430 DENTAL CARIES 

treated. If further treatment be desired, or be impossible until 
the perforation is disposed of, metal or wooden pegs (the Downie 
broach reamers will serve) are placed in the canals and a reasonably 
thin layer of copper amalgam is built about the pins and over the 
perforation. A slight movement of the pegs will permit their with- 
drawal, leaving openings in the amalgam through which the treat- 
ment may be subsequently conducted. The amalgam is then 
allowed to harden (Fig. 378). To carry on the treatment while 
hardening, formocresol on a cotton pellet may be inserted over the 
openings in the amalgam and sealed over with soft cement. N 

After canal filling the canals may be further reamed for screws or 
pins, which are inserted and the operation completed with amalgam, 
or zinc phosphate and amalgam if the condition of the crown admit 
of it; or, if crowning be required, this is arranged for in the building 
up with amalgam. 

A long perforation at a bifurcation may practically divide molar 
roots. This is to be made a complete division after treatment of the 
canals. Each section may be fitted with a pin and amalgam stump, 
to which a gold barrel is fitted. The barrels are each given an occlu- 
sal face, or the two a common occlusal face, and soldered together 
(Fig. 379). 

If one root be unsuitable it may be extracted and the other used 
as a foundation for a cantilever crown, a spur from which rests 
slightly upon the occlusal face of the adjoining tooth (Fig. 380), or 
the crown may carry a spur which rests in an inlay or filling in the 
adjoining tooth. 

A smooth plaque of low-heat, white gutta-percha (not temporary 
stopping) makes an excellent covering for a perforation. It is made 
larger than- the opening covered, warmed, pressed to place, and the 
edges sealed with a hot burnisher. The covering filling will retain 
it in position. The approach to the perforation should be widely 
funnelled to permit a ready adaptation. A splendid covering for 
accessible perforations is found in oxyphosphate of copper cement. 
The opening should be funnelled, the parts dried thoroughly and 
the cement properly mixed can be painted over the orifice, adhering 
tenaciously to the tooth and soft tissue without pressure. It exer- 
cises an antiseptic influence. If sepsis occur, the resulting abscess 
will occur opposite the perforation, or in some cases create a small 
pocket similar to a pyorrhea pocket. In all cases judgment must 
be exercised, and the attempt to conserve unsuitable cases avoided 
(Fig. 381). (See also Chapter XX.) 



THERAPEUTICS OF LOSS OF CROWN BY CARIES 431 

THERAPEUTICS OF LOSS OF CROWN BY CARIES. 

If the portion of crown left after excavation be self-sustaining, 
but Incapable of retaining a filling in the cavity, pins or screws 
may be placed in the root canal or the pulp cavity may be enlarged 
and made retentive. A filling is then built about or into the anchor- 
age so made. At times the remainder of a tooth crown will support 
a hollow metal crown. 

When the carious crown has broken away or filling has become 
practically impossible or undesirable, the original beauty or useful 
form of the tooth may be approximately restored by means of one of 
the many forms of dowelled porcelain crowns, specially constructed 
gold and porcelain crowns, or all-gold, hollow-metal crowns, or a 
broad band may be adjusted and filled in with amalgam after setting 
with cement, or where a portion of crown only remains soft amalgam 
may be used inside of the band to make the adaptation, and the band 
then filled in, completing the work on the side at which the band 
has no cervical adaptation. These operations have been successful 
for years, if the remnant of crown has any supporting ability. 

If an anterior root be so hollowed out by caries as to be incapable 
of supporting a dowelled crown, with or without a cast base, it may 
be extracted, and the operation of transplantation performed, or, 
later, an implantation may be made. 

In the former operation the existing alveolus is enlarged if necessary 
to accommodate a tooth; in the latter operation a new alveolus is 
created by means of appropriate trephines and bone reamers. The 
tooth is -to be prepared as for replantation (which see). 1 

If teeth have been lost by extraction, the spaces created may be 
filled by means of bridge-work or plates of various sorts. 

By common consent crown and bridge-work is considered a 
special department of dentistry . 

Therapeutics of Loss of Roots by Caries. — This occurs in several 
ways : 

1. After loss of the crown and the extension of the carious process 
into the interior of the root. In the later stages this root is rendered 
valueless for crowning purposes, and should be extracted. In some 
cases a transplantation operation would be warrantable, as in case 
of a single incisor, the other teeth being relatively sound. (See above.) 

2. If an artificial crown has been so placed as to expose the joint 
to , caries, the process may proceed to a considerable extent, but 
does not necessarily involve the root interior, owing to the presence 

1 For methods of implantation, see American Text-book of Operative Dentistry. 



432 DENTAL CARIES 

of the pin. Filling with amalgam or other plastic, or the recrowning 
is demanded if feasible. The gum having grown in, much packing 
out may be required; ablation may be required as well. 

3. In some cases penetrating cervical caries will cause a partial or 
complete amputation of a lingual or buccal root of an upper molar, 
or, possibly, a bicuspid. The pulp, of course, will have died, at 
least at the carious area. 

The cavity of decay should be cleansed and undercut, and an 
occlusal tap made for free entrance to the canals. The canals are to 

be reamed with Kerr broaches. The canal 
Fig. 382 of the decayed root is to be enlarged with 

Kerr root reamers, after which everything 
is to be dried ; a canal probe, or the largest 
reamer used, which may have wax in the 
spaces between the blades, is passed through 
the tap across the cavity into the farther 
portion of the root canal. Good amalgam 
is to be thoroughly packed into the cervical 
cavity and hardened by wafering. When 
nearly set, the filling is supported against 
dislodgement and the canal probe is care- 
Method of restoring lost fully withdrawn. After appropriate steri- 
ZuidTav^moJ retention Nation of canals with formalin solutions, 
form than shown, a, amalgam, the canal is filled. If the decay has been 

severe, and fracture threatens, an iridio- 
platinum pin is to be fitted into the involved canal and the crown 
tap and the pin used as the canal former while filling the cavity. 
Later after sterilization it is cemented into the canal, thus strength- 
ening the root against a threatened fracture. 

If actually separated by decay, excavation will make an open joint, 
which should be filled with amalgam after the pin has been run 
through the tap into the root. If this operation does not seem 
feasible, it is better to extract the separate root portion and trim the 
stump, as in ordinary root amputation. 

While the retention of an amputated root is seldom demanded, the 
editor has several in satisfactory use. The prevention of a threatened 
fracture is more often demanded. (See also Heteroplasty.) 

CARIES OF THE TEMPORARY TEETH. 

Caries of the temporary teeth differs but little from that of the 
permanent teeth. The pulp cavities are, however, relatively larger, 
and the intensity of the carious process often causes rapid exposure 




CARIES OF THE TEMPORARY TEETH 433 

of the pulp. Owing to the fiat character of the approximations of 

the teeth, there is often more approximal than occlusal caries, and 
the cavities often have weak peripheries. 

Children have a fear of dental offices, excited by unpleasant experi- 
ences or the talk of their elders, and they do not mention slight pain 
such as that excited by hypersensitive dentin. There is, however, 
abundant evidence that the dentin of the temporary teeth may be 
hypersensitive. In cavities of simple nature the fillings indicated 
for adults serve if the operations are well borne. 

The shapes of the teeth, the restlessness and fear of the little 
patients, and the free flow of saliva indicate, for the most part, the 
use of plastic fillings, though the rubber dam may often be readily 
used. In deep cavities not exposing the pulps, the methods employed 
for adults, of varnishing or insulating with gutta-percha and the 
subsequent use of zinc phosphate as a lining under metal fillings, 
arei ndicated. (See p. 421.) Certain occlusal cavities having small 
orifices and large interiors are well, and often permanently, filled 
with pink gutta-percha. Zinc oxid and eugenol made into a stiff 
paste often fills cavities acceptably, and lasts as well as oxyphos- 
phate unless it is too freely masticated upon. 

If cavities are observed before pain has been complained of, and 
prompt and quickly subsiding response to applications of cold water 
is obtained, indicating a normal pulp, the cavity 
should be excavated, with more regard to re- FlG - 383 

moving the marginal caries than to thorough 
excavation, dried, and an application of a 20 
per cent, solution of silver nitrate made for a 
few minutes, the cavity being subsequently 
filled. 

In cases of adjoining approximal cavities „ , 

. . -.. .,. , ° :/ r - , , Mode of preparing 

there is a disposition lor the affected teeth to approximal cavities. 
press together and lessen the size of the dental 

arch. Bonwill advised as a practice, followed by uniformly good 
results in such cases, to cleanse the cavities (Fig. 383) and insert 
masses of pink gutta-percha base-plate. The constant biting upon 
the gutta-percha causes a separation of the teeth, which increases 
the size of the arch and affords additional space for permanent 
successors. Hollingsworth introduced the idea of placing a small 
piece or cap of metal at the cervix, bridging the interdental space. 
A bit of gutta-percha is to be placed on the under side of the cap 
to make a gutta-percha adaptation; then more is built over it. Bon- 
will advised that before the gutta-percha masses are inserted, small 
pieces of blotting paper saturated with carbolic acid be laid against 
28 v 




434 DENTAL CARIES 

the dentinal walls and the gutta-percha be packed over them. The 
more efficient and persistent antiseptic silver nitrate may be applied 
instead of the carbolic acid. Kirk advises that asbestos felt be 
heated to destroy any organic matter present in it which might 
combine with the silver, and then be soaked in a saturated solution 
of silver nitrate, dried, and kept in dark bottles away from the light. 
Small pieces of the prepared felt may be used as described. With 
cavities as good as shown in the illustration, wedging and contouring 
each tooth with amalgam, after the use of silver nitrate and varnish, 
is quite admissible after making suitable retention. There is no 
reason why occlusal extension for retention should not be made. 
The conditions will determine the choice of materials. 

Fig.^384 




Right upper temporary molar disked lingually and filled. 

The silver-nitrate method is particularly applicable to shallow 
cavities in which excavation for filling is impracticable. The dentin 
surface is cleansed and dried, and the fused silver nitrate is rubbed 
upon the surface. This may be done after the method of Craven: 
a platinum wire is dipped into the powdered salt and held over a 
flame until the powder fuses into a button. By this means applica- 
tion can be directly and accurately made. The arch is apt to become 
somewhat contracted, and food is liable to wedge between the teeth. 
Combination fillings of zinc phosphate or oxyphosphate of copper 
and amalgam are of advantage in case of frail walls. 



CARTES OF THE TEMPORARY TEETH 435 

For the anterior tooth silicate, zinc phosphate, and gutta-percha 
fillings are useful, and for the posterior ones Ames' oxyphosphate 
of copper servos a good purpose. 

Caries is very liable to occur upon the approximal surfaces of the 
second temporary and first permanent molar. If the former be 
found largely decayed distally, the latter will usually be found decayed 
on the mesial surface. Amalgam in cavities well extended buccally 
and lingually, or gutta-percha, serves well until the second temporary 
molar is lost, when a good gold filling may often be introduced 
before the second bicuspid erupts. 

Well-contoured fillings must be inserted in such a case. As a 
preventive measure during eruption of the first molar, the second 
temporary molar may be disked to the form shown in Fig. 384. 

If incipient or simple decay has occurred on the two teeth, or 
even the second molar alone, it is then best to wedge the teeth apart 
and to make a disk separation (on the temporary tooth only) from 
the lingual or buccal side, or both, and to contour the filling even in 
exaggeration, so that a minimum of contact shall exist. Any sur- 
face of dentin exposed by the disking should be included in the cavity, 
or, if this be not possible, then it should be rubbed with silver nitrate. 

Such surfaces should be carefully observed at regular intervals; 
indeed, if prophylaxis can be regularly instituted early and before 
caries of the first permanent molar, much good will be done. 

The pulp diseases resulting from caries of the temporary teeth will 
be considered with those of the permanent teeth. If the temporary 
teeth be so badly decayed as to be hopeless, so far as filling is con- 
cerned,' they should be extracted. Occasionally the encircling of the 
teeth with pure gold bands cemented to place, or filled in with amal- 
gam is good practice. 

In the main the temporary teeth, especially the molars, should be 
filled with some view to the longevity of the fillings, as they often 
have to do service for years, and the general health of the mouth is 
improved. 

The child should always be treated with kindness and truthfulness 
to establish faith, yet with sufficient firmness to command control. 

Under no circumstances should the child be given an excessive 
dread of dental operations, or be broken by nervous shock, as this 
attitude defeats the object sought. 

In one extreme case in which the child had never endured dental 
work, chloroform followed by ether was given and fifteen plastic 
fillings inserted. N 2 and O might be used for the purpose. 



436 DENTAL CARIES 



RECURRENCE OF CARIES. 

Passing over, as disproved by Miller, the theory of Palmer, that 
caries recurs about fillings as the result of electric action, it may be 
stated, as proved by scientific and clinical experience, that it recurs 
because after teeth have been filled, conditions exist which may favor 
the collection of microbic plaques and stagnant food material even 
more strongly than the original conditions, and that when recurrence 
has been prevented, the work has been done in such a manner as to 
prevent such collections 

The specific defects which favor the formation of bacterial plaques 
may be epitomized as follows: 

1. Lack of approximal contact (food wedging between teeth). 

2. Roughness of the filling at an otherwise good approximal con- 
tact point which menaces the approximating tooth or the margin of 
the cavity by causing food retention and the spreading of microbic 
plaques. 

3. Unremoved excess of filling material at margins producing a 
ledge which collects food, etc. The edge of a crown may act in a 
similar manner. An excess well beneath the gum is more apt to 
produce gingivitis than caries. 

4. Exposure of the cavity margin due to lack of covering by the 
filling material, whether not properly placed, flaked away, or due to 
fracture of margin during the filling process or subsequently thereto. 

5. Exposure of the cavity margin due to shrinkage or shifting of 
the filling material. The use of material not enduring mastication 
in places subject to it; the washing out of cement from the joint 
of an inlay or combination filling or dowelled bandless crown has 
much the same effect, though often much delayed. 

6. Solubility of the filling material, permitting the cavity wall to 
become exposed. 

7. Roughness of tooth surface, produced by polishing fillings with 
rough approximal trimmers, coarse grit strips, disks, or wheels. 
Exposure of dentin by overpolishing may be classed with the above. 

8. Lack of hygiene of surfaces which tend to decay, partly due 
to lack of extension of cavity margins. Even poor margins, if well 
extended, may not decay, whereas existing at or near contacts they 
are menaces. Lack of extension of approximal cavities often causes 
failure, through failure to include all carious enamel. Lack of exten- 
sion of a filling into a fissure adjoining it, which fissure may be 
decayed or invite subsequent decay. Lack of extension of labial 
cavities sufficiently under the gum cervically and in the mesial and 



PROPHYLAXIS OF CARIES 437 

distal direction, leaves a tissue vulnerable to microbic plaques if not 
already attacked superficially. 

Treatment. — The treatment of recurrent caries does not differ 
materially from that of primary caries. 

Repairs to obliterate crevices, breaks, or new decays may at times 
be made; but so often is it the case that apparently slight recurrences 
are found after removal of the filling, to involve the entire cavity wall, 
that the only sound recommendation applicable to all cases is that 
the filling be removed and the cavity reprepared and refilled. The 
exception exists when, after the new cavity of decay is all excavated, 
the adaptation of the filling is seen to be perfect. Decay at two or 
more points of recurrence not subject to accurate repair, or general 
inferiority of the filling should condemn the entire piece of work. 

PROPHYLAXIS OF CARIES. 

If the factors, or even one factor of caries be removed from the 
mouth, caries cannot occur. The microscopic plaques and fermen- 
table food substances acting as the causes of caries should, therefore, 
be kept from collecting upon the teeth. The longer they remain, 
the further they may spread laterally over the tooth surface. 

In the absence of absolutely exact knowledge of the relation of 
general systemic conditions to the production of microbic plaques, it 
may be said that the general health should, if possible, be maintained 
by the correction of any morbid body state, as, without doubt, perfect 
good health is a corrective of morbid oral secretions. (See p. 356, etc.) 

Apart from this, oral cleanliness is of great importance, not only 
for the health of the teeth, but of the gums, and, indirectly, of the 
stomach and intestines, which can but be affected by unhealthy oral 
conditions. Thus while the general health may influence the mouth, 
the mouth may influence the general health. 

It has been noted that caries is markedly lessened in well-kept 
dentures. 

The first step in the prevention of caries is the removal of all 
possible causes of bacterial plaque formation. Cavities should be 
obliterated by means of exactly adapted, perfectly contoured, highly 
polished, insoluble (in so far as utilizable) fillings, the margins of 
which are extended into areas subjected to friction by ordinary 
forces, such as food excursions, brushing, etc. Departures from this 
principle are to be made for well-judged reasons only, and when 
made prophylaxis must be more rigorous. 

Some dentists pursue the policy of filling only the larger cavities 
existing in a mouth, the others being neglected until a subsequent 



438 DENTAL CARIES 

period. Such a method is to be condemned as being a neglect of a 
plain duty and as tending to the propagation of caries in the mouth. 

Periodical examinations should be made at short intervals, pref- 
erably at the time of cleansing, for cavities of decay, roughness of 
filling margins, or accidents to the same. By these means the 
soil may be rendered unsuitable to the growth of caries fungi, and 
their localization at the contacts and other favoring spots is largely 
prevented. 

Silver nitrate, 40 per cent, to saturated solution, may be applied to 
surfaces likely to decay, as sulci, contact points, etc., as a means of 
prevention in mouths subject to same. 1 As a systemic and local 
prophylactic, the diet may be modified (see p. 361). 

The presence of cavities, calculus, and pyorrhea alveolaris in the 
mouth all tend to cause infection of the digestive tract, with produc- 
tion of inflammatory (catarrhal) . disturbance, and to cause infection 
of parts in close association with the teeth as well. 

Undoubted cases of septic intoxication and infection from decayed 
teeth and other oral conditions have been reported, the connection 
having been shown by their cure after removal of the local cause 
alone; in other cases the parts (as the stomach) having the secondary 
infection well implanted, have required special treatment in addi- 
tion to the removal of the primary exciting cause. 2 (See Systemic 
Effects of Pyorrhea Alveolaris.) 

The loss of masticatory efficiency due to caries or the associate 
pain has a direct bearing upon insalivation of food and upon gastric 
digestion, though in this connection bacterial infection may play a 
part. 

School children who suffer much from caries are apt to be less 
proficient in their studies than normal children, the effect being 
probably due to that of disturbed digestion upon metabolism and 
thus upon mentality in general. Pain, of course, is a direct cause 
reducing vitality in various ways and causing loss of time and atten- 
tion to the duty of study, etc. The following quotation from a 
tabulation 3 shows typically the effect of dental normality upon 

1 L. C. Bryan and others. 

2 Hunter: International Dental Journal, 1899, abstract from Transactions of 
Odontological Society of Great Britain. 

In an address at McGill University, Montreal, Hunter, 1910 (see Dental Brief, 
November, 1911). reaffirms extensive experience with gastritis, septic anemia, septic 
endocarditis, etc., as the result of oral sepsis in which decayed roots and extensive 
dental work, (bridge, etc.), covering septic conditions were cured by removal of the 
cause. While caries was not separately considered, it must be seen that caries is 
largely responsible, as the inception of the conditions through pyorrhea is also 
responsible. 

3 Dental Brief, 1911. Tabulation of the Effects of Dental Caries on the Mental 
Powers of the Dental Class in Marion School, Cleveland, Ohio. 







Per cent, of 


Present. 


Diffeience. 


gain or loss. 


66.6 


00.05 


00.07 


90.7 


16.50 


22.22 


63.0 


17.00 


36.95 


92.0 


33 . 00 


55.93 


60.5 


19.00 


45.78 



DAILY CLEANSING OF THE TEETH 439 

mental powers. It has the lowest gain, which ranged from about 
32 to about 918 per cent. 

Beginning. 

Memory 66.65 

Spontaneous association . . .74.25 

Addition 46.00 

Association by opposite . . . 59 . 00 

Quickness and accuracy of perception 41.50 

Total gain .... 32.162 per cent, after deducting the losses. 



Insomnia and a variety of other metabolic ills have been shown 
to be due to carious teeth and the sepsis associated, by the prompt 
or gradual recovery upon removal of the teeth. How many thous- 
ands of individuals suffer from partial sepsis, in entire ignorance and 
possibly without actual discomfort can only be conjectured. It is 
exceedingly difficult to state positively that a metabolic disorder 
is due to the state of the mouth, unless a microscopic examination 
from a separate locality demonstrates identical bacteria present. 
Even then the therapeutic test must decide. Therefore general 
deductions must govern advice. In all cases it is w T ise to put the 
mouth into a hygienic state and, if necessary, add such other therapy 
as the systemic condition demands. 

The evils attendant upon sepsis are to be pointed out to patients 
who have often a seeming indifference to conditions ranging from 
simple uncleanliness to loathsome filth within the mouth, which 
would alarm them if existing in any other part of the body. Aside 
from all considerations of health or tooth integrity, it is poor economy, 
and especially for poor people, to neglect these measures which are 
largely applicable. The prophylaxis of the teeth apart from periodical 
cleansings is a matter for careful instruction and exhortation of 
patients who are apt to be persistent backsliders. Indeed, it is the 
opinion of the w T riter that most patients accept the validity of the 
arguments herewith presented and then persistently neglect or even 
frankly refuse to carry out the treatment. It is therefore no surprise 
that caries persists. The deduction may be made that the cleansing 
of teeth at spots that ordinarily do not decay is nearly equivalent 
to no brushing at all. 

DAILY CLEANSING OF THE TEETH. 

A small, well-made, fairly stiff brush, having its brushing surface 
serrated, is to be grasped in the palm of the hand with the ball 
of the thumb placed upon the back of the handle, or exactly the 
reverse, according to the movement desired. The bristles are to 



440 



DENTAL CARIES 



be passed over the buccal and lingual surfaces of the teeth, from the 
gum toward the occlusal surfaces, by means of a dexterous, wiping 
motion imparted by a turn of the wrist. Figs. 385, 386, and 387 



Fig. 385 




Fig. 386 




Fig. 3S7 




by S. Blair Luckie, show this. This cleanses the interproximal 
spaces so far as accessible to the brush. By a light to-and-fro 
motion, spreading the bristles over the cervices, the lingual and 
buccal cervices are freed of soft deposits which occur after each meal. 



DAILY CLEANSING OF THE TEETH 441 

Unless the gums be actually torn, this light friction is not injurious. 
Special attention is to be paid to the buccal surfaces of third molars, 
which arc often ignored even by conscientious patients. This is due 
to a habit of giving a downward sweep of the brush-tip, which escapes 
the rather upwardly placed third molar. 

The lingual surfaces of incisors are cleansed by means of the 
tip of the brush. In cases of advanced recession of the gum about 
incisors, a brush with all the bristles except those of the tip cut away 
(and the stubble ground down) is advantageous. This is also useful 
for the lingual surfaces of bridge-work. Occlusal surfaces are to be 
freely brushed. Brushes of this form can be purchased. 

A light brushing after each meal imparts to the mouth a pleasing 
sense of cleanliness, which has a good moral effect upon the patient, 
and removes from about the teeth much fermentable material. 

The teeth should be thoroughly brushed upon retiring, to remove 
any debris about the teeth. A small rubber band should be 
stretched between the teeth, the inner end released, and then 
drawn through the interdental space, wiping the approximal sur- 
faces and embrasures. This places the mouth in a fairly aseptic 
state for the night, during which the oral fluids are at rest and 
less interfere w T ith fermentation, or neutralize its products. The 
brush itself should be sterilized after using. A good glass brush- 
holder is sold which has a small portion of paraform placed in the 
lower part, and is capped with a metal screw cap. In this the brush 
may remain until again needed. 

Before breakfast the teeth should again be brushed. 

Once a week the patient should rub tooth powder over the inter- 
proximal spaces, and carry floss silk between the teeth and rub the 
approximal surfaces, with the object of removing any bacterial 
collections upon these surfaces. 

The floss silk should not be forced into the gum, as this will injure 
the gum margins and force infected material into it, but should be 
first carried gently beneath the gum, wrapped half around the tooth, 
and then sawed up over the contacts and be brought out from 
between the teeth. It should be reintroduced at the same interspace 
and the adjoining tooth polished. This use of floss still leaves at 
the middle of the buccal and lingual cervix a point often uncleansed 
(see Fig. 364). The use of the brush to accomplish this should 
be taught, otherwise cervical caries may supervene (see p. 384). 

The lingual surface of lower incisors may usually be accurately 
flossed by throwing the floss around a single tooth, then crossing 
the strands and pulling on each alternately. This cleanses the 
entire circumference at the cervix, as the floss tends to go cervically 



442 DENTAL CARIES 

under such a manipulation as is shown by its use with the rubber dam. 
If there is any difficulty in the use of floss, it is due to faults about 
the approximal surface which should be remedied. In cases of lower 
incisors collecting calculus readily this may have to be done daily. 

The twisted-wire bodkin shown in Fig. 389 is very valuable as a 
means of threading the floss through a bridge space. Being readily 
bent into a half-circle it returns toward the lips so as to be readily 
grasped. It should be bent in line with the flatness of the eye. To 
make them, take the temper from a thin shank like that of an old 
Gates Glidden drill, bend it into the form of a button-hook; over 
this loop a six-inch length of fine regulating wire. Revolve the hook 
in the engine and run the wire through the fingers of the left hand. 

The periodical cleansing or prophylaxis suggested by D. D. Smith 
involves the monthly rubbing down of all surfaces accessible, to a 
wedge-shaped, wooden polishing point carried in a Jack porte. 
Powdered pumice is the abrasive suggested. The point is to be gently 
insinuated beneath the free gum margin for the purpose of effecting 
a cleanliness there, which shall prevent collections liable to produce 
pyorrhea alveolaris. (See Fig. 645.) 

This method may be supplemented by a careful rubbing down of 
contact points and embrasures by means of floss silk, charged with 
powdered pumice as an additional precaution against approximal 
caries. 

Fig. 388 




Simple porte-polisher. One, shoe peg trimmed. 

The slight cleansing apparently required after a few visits is a 
strong argument in favor of these prophylactic cleansings, and chalk 
may be substituted for the pumice. In case of fairly clean mouths, 
free of other disease than caries the patient may be instructed in 
the use of a shoe peg sharpened to a point, held in a simple porte- 
polisher, such as a tube of thin nickelled brass bent at one end to an 
angle of 45 degrees (Fig. 388), and the prophylaxis by the operator 
executed three or four times a year only. This wood point is useful 
in cleansing the lingual surfaces of bridge-work. 

It is exceedingly difficult to instruct patients in the proper use 
of the wood point, but once properly instructed the results are 
little short of marvelous. In use it is to be held in the hand as 
though using the Spencerian system of penmanship. The third 



DAILY CLEANSING OF THE TEETH 443 

and little finger rest upon the chin or teeth as a fulcrum. The 
point is first adjusted at the distal of the third molar and with a 
rocking motion of the hand it is drawn along the cervix. The rule 
is to "keep" on the tooth but "feel" the gum. Jumping from the 
buccal of one tooth to another is to be avoided. The point should 
be deliberately but gently drawn (not rubbed), until it rests in the 
interspace. Next the fulcrum fingers are slightly shifted and the 
next tooth cleansed. 

Fig. 389 




Flexible wire bodkin slightly enlarged. 

When the anterior teeth are reached, the patient should begin 
again at the third (or last) molar of the opposite side. The motion 
is repeated upon the lingual surface. In no case should sight be 
depended upon. The sensation of contact is the best guide. As a 
means of instruction of the patient, tincture of iodine and alcohol 
equal parts should be applied and then washed off with water. The 
films will stain for a short time, during which the effect of the fric- 
tion of floss and stick and the inefficiency of the usual brushing 
can be demonstrated. If desirable, the patient may occasionally 
use the stain as a means of self instruction. 

The Dentifrice. — There is no contention as to the value of friction 
and the removal of the factors of caries, but of late the character 
of dentifrice to be used has been brought into question. 

Pickerill has contended that antiseptics are of doubtful value and 
that ordinary alkaline dentifrices depress the flow of saliva and that, 
on the other hand, an acid dentifrice, as acid potassium tartrate in 
1 to 200 solution, increases the .flow of alkaline saliva, which being 
continuous neutralizes any acid formed. As aside from a detergent 
action, alkalinity is the object sought in a dentifrice, the method 
seems rational, especially as he has found that the acid does not injure 
the teeth. 

Of his formulae the following is said to be the most agreeable: 

1$ — Potassii bitartratis (P. tartratis acidi, B. P.) . . gr. ij 

Acidi tartarici gr. j 

Olei limonis Tfl. iij 

Glusidi (saccharini) gr. \ 

Aqua? ad fgj — M. 



444 DENTAL CARIES 

The contentions of Pickerill are based upon his observations of 
immunes, and experiments which curiously enough do not seem to 
include definite experimental applications to any particular indi- 
vidual susceptible to caries. It is seemingly becoming the fashion 
to claim that prophylaxis is a failure (Pickerill admits its occasional 
value), which will not be admitted for a moment by any one who 
has conscientiously performed it each three months, or oftener, with 
reasonable assistance from the patient (see footnote p. 358). Anti- 
septics are also denied a value, but even Pickerill admits their value 
in oral sepsis, so why can they be valueless in caries. They produce 
a disturbance in the medium, slight changes in which are known to 
affect bacteria, a fact taken advantage of by Pickerill as a claim for 
acid value. If disturbance of medium is of value, the frequent break- 
ing up of plaques theoretically should be of immense value and in 
practice so proves. 

Antiseptics have been shown to reduce general oral infection to 
a possible minimum when oral cleanliness is conjoined with their 
faithful use, but without exact prophylaxis cannot be depended upon. 

The writer has found phenol sodique, 1 to 7 of water, a useful 
adjunct in this connection and as an occasional germicide to 
promote the action of milder antiseptics, the following mercuric 
chloride wash used for the space of two minutes is valuable: 1 

ty — Mercuric chlorid gr. vj 

Thymol gr. ij 

Menthol gr. v 

Oil eucalyptus gtt. x 

Glycerin fgij 

Alcohol fgij 

Auqae gaultherise q. s. ad. Oij — M. 

S. — Use as directed as mouth wash. 

The writer has found much value in the use of a potassium chlorate 
paste. This certainly has kept black stain from teeth which usually 
accumulated strong evidence of it within two weeks of prophylaxis, 
and caries is apparently much lessened by its use though prophy- 
laxis is a confusing factor. Potassium chlorate has been condemned 
by dentists of high standing as systemically injurious, but whether 
such small doses as might be swallowed after tooth cleansing could 
be injurious has not been scientifically showm. On the other hand 
experiments 2 have been made on puppies which received thirty grams, 
daily for six weeks, were then killed and no renal lesions were found ; 
the gastric mucosa showed no signs of irritation nor the blood any 
methemoglobinemia, and the animals showed normal growth. While 

1 C. R. Jackson, Dental Summary, 1904. 

2 Medical Brief, December, 1912. 



DAILY CLEANSING OF THE TEETH 445 

large doses may have been injurious to humans this is entirely different 
from minute residue in the mouth. As a matter of fact, if the 
mouth be washed out with water no appreciable toothpaste need be 
swallowed. 

The use of chewing gum after meals has been of value in suscep- 
tibles. Either it acts by friction, removing fermentable food or by 
promoting a free flow of saliva; perhaps in both ways. 

Whether, however, it shall be best in the future to prescribe 
a weak organic acid as a dentifrice and trust to the flow of alkaline 
saliva or use a w r eak alkaline wash, as lime-water one-half strength, 
or even an alkaline tooth pow r der or paste must be decided by actual 
clinical experiment upon susceptibles, as immunes are valueless for 
observation unless they lapse from immunity. Even here the credit 
must not be given altogether to the acid treatment side of the con- 
tention unless prophylaxis is eliminated. In brief, the w-hole sub- 
ject requires intelligent ventilation. We have to thank Pickerill 
and Gies, working on this line, for at least a new departure in our 
thinking regarding dentifrices. 

By these means centres of infection are removed, and the problem 
is reduced to the care of the superficies of the teeth. Calculus should 
be thoroughly removed, the teeth highly polished and kept polished. 
This operation mechanically removes the plaques. 

To prevent their return, daily cleansing of the teeth by the patient 
has always been practised, and a thorough cleansing once a month 
or oftener by the operator has been shown by D. D. Smith to be 
highly efficacious. The patient should be instructed regarding the 
location of the plaques producing dental disease. A good method is 
to apply tincture of iodin to the teeth, then douche them with water, 
which removes the iodin from the clean part. The teeth wall gener- 
ally then look like Fig. 321, which, while a figure of decay, will take 
the place of a special illustration. While thus stained the effectiveness 
of floss, etc., can be readily demonstrated. Inasmuch as caries is 
usually prevented by a thorough monthly prophylaxis followed by 
oral hygiene at the hands of the patient, it follows that if the bacterial 
plaque is frequently disturbed the most important link in the chain 
of factors is eliminated. Even if a systemically produced carbohy- 
drate should be shown to be a factor as food supply for bacteria, 
it can produce no injury alone, while it is probable that bacteria 
plus extraneous carbohydrate is competent to produce caries. 

Finally a dietary should be outlined which shall be proper for 
general health, shall reduce the carbohydrate element remaining in 
the mouth (as candy and cracker consumption betw r een meals), 
and shall induce a flow of alkaline saliva after meals (see p. 361). 



446 DENTAL CARIES 

PROPHYLAXIS IN SYSTEMIC DISEASE. 

During a prolonged illness, seasickness, pregnancy, etc., the pro- 
phylaxis of the teeth should be as rigidly enforced as possible as a 
means of preventing decay of the teeth and sepsis of the mouth. 

It has been shown that during pregnancy osteomalacia may occur, 
and that it represents a demineralization by decalcification of the 
bones of the mother. Whether or not this may influence caries of 
enamel is not certain, though acid secretions occur from the gum 
margins, but there is no reason why the resistance of the fibrils of 
the dentin should not be lessened, or even that the dentin may not 
be to an extent demineralized, as positively claimed by some accurate 
observers (Black to the contrary). An excessive osteomalacia may 
be held to represent a deficiency of osteogenetic nutritive material 
for the child. This would lead to an inferior development of the 
child's temporary teeth. 

Any abnormal condition of the mother should be corrected, if 
possible, in order that her general nutrition and that of the child 
may not suffer. 

Probably upon the congenital constitution of the child depends 
much of its future susceptibility or immunity to caries. 

Accepting the decalcification theory of osteomalacia, the use by 
the nursing or gravid mother of mild alkalies internally, such as a 
tablespoonful of lime water repeated, and the use of lime-containing 
foods, as the cereals, and mineral waters as beverages, cannot but be 
of values as antacids furnishing a neutralizing agent for the acid, 
while the lime probably enters into the development of bone (Hare), 
and, therefore, would be useful in supplying, via the placenta, 
mother's milk, and later the child's food, the element needed for the 
development of teeth. The use of glycerophosphate of lime and soda 
has been suggested. 

The teeth should receive all needful care during pregnancy, that 
the mother should not suffer pain, but work should be of a temporary 
nature, if necessary, to avoid shock, especially at about the third 
month of gestation. Attention has been called to the fact that 
during menstruation a systemic hyperacidity exists, which can be 
combated by the use of lime internally and milk of magnesia or 
lime water locally. 

In the care of the teeth during pregnancy the effect of the hydro- 
chloric acid vomitus upon the teeth should be considered, an alkaline 
wash such as lime water or bicarbonate of soda solution to be used 
after the vomiting. The same would be true of seasickness and after 
the use of any acid drug or foodstuff, such as tincture of ferric chloride 
or buttermilk in case the latter is a constant diet. (See p. 354). 



SECTION IV. 

DISEASES OF THE DENTAL PULP. 



CHAPTER XV. 
CONSTRUCTIVE DISEASES. 

Diseases of the dental pulp are both acute and chronic. Accord- 
ing to the anatomical features, they may also be divided into con- 
structive and destructive. The acute diseases are usually destruc- 
tive; in the chronic, structural and constructive changes are com- 
monly noted. Constructive diseases of the dental pulp are those 
attended by the formation of deposits of new masses of calcific 
substance. Destructive diseases are those which cause retrogressive 
and necrotic changes in the tissues of the pulp. The essential differ- 
ence between the two classes of disease is in the mode and character 
of the degeneration — the one is acute, the other chronic. 

Pathologically there is no abrupt line of demarcation between 
diseases of the dentin and those of the pulp, as the dentinal tubules 
contain the fibrillar prolongations of the odontoblasts of the pulp. 
Effects produced upon the fibrils cause, therefore, a pulp reaction 
which may lead either to a constructive or destructive activity 
according to the grade of hyperemia or inflammation set up. 

As infection may travel via the tubules, even septic inflammation 
may result before the pulp is exposed. 

Moreover, after constructive changes which are accompanied by 
more or less atrophy and degeneration, the pulp may undergo the more 
acute destructive changes. While the exact relations between symp- 
toms and pathology are not all worked out and the symptoms are 
often obscure, due to the fact that the pulp is without the sense of 
touch or exact location, and, therefore, the pains induced are reflected, 
as a rule, yet clinical observation and the x-rays have done much to 
relate the symptoms and pathology, and one must depend upon 
these and applied tests for at least a tentative diagnosis, of which 
confirmation may be sought. 

(447) 



448 CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

The pathological conditions of the pulp are judged by the phenom- 
ena induced by applications of air or water of varying temperatures, 
and by the presence of certain appearances of the tooth, which, taken 
with the symptoms and tests, lead to a fair inference of the disease 
present. 

It was pointed out by Black 1 that if a healthy tooth be isolated by 
a double layer of rubber dam, and a jet of water at a temperature of 
40° F. be directed against the tooth, a paroxysm of pain is produced. 
A jet of hot water will also induce a similar pain, and if the patient's 
eyes be shielded no difference in the sensations is noted; that is, 
the pulp responds to thermal stimuli, hot or cold, indifferently. The 
organ is accustomed to variations of temperature between 60° and 
105° to 110° F., and within this range, in a condition of health, 
takes no apparent cognizance of this degree of change. 

With a decrease in the amount of dentin covering the pulp — e. g., 
with the advance of caries — the reaction to thermal stimuli increases 
in promptness until, when the pulp is nearly exposed, the response is 
immediate. As the pulp irritation increases there is prompt response 
to lesser degrees of temperature change, until finally the pulp 
responds immediately to water at a temperature but a few degrees 
below or over the bodily temperature, 98.6° another feature makes 
its appearance; instead of a sharp contraction pain, applications 
of moderate thermal stimuli are followed by a heavy, throbbing 
pain. Later, similar pains occur in the absence of tangible external 
sources of irritation. In conditions of abscess intense pain is later 
caused by hot applications, and cold applications afford relief. 

In pulp degeneration the response to thermal stimuli may pursue 
the opposite course. The normally prompt response is followed by 
delays in reaction, until it is only after the continued application of 
cold to the exterior of a tooth that a paroxysm of pain is induced. 
In these cases there follows after a relatively long time an increasing 
response to heat, as in the former instance, the reaction occurring 
only upon decided or prolonged heat stimuli. Following upon the 
period of increased response to heat, in both cases there comes a 
period of quiescence, in which there is no response whatever to 
applications of intense cold, even that produced by the evaporation 
of a spray of ethyl or methyl chlorid — i. e., the sensory function of 
the pulp is paralyzed. This only in intense venous hyperemia or 
degeneration. 

These are the available subjective evidences of the pathological 
conditions of the pulp ; while they indicate with a degree of accuracy, 

1 American System of Dentistry, vol. i. 



TUBULAR CALCIFICATION 449 

useful in clinical work, the alterations in the pulp, the exact relations 
between the reactions and the morbid anatomy of the organ are not 
entirely clear. It is assumed that, in consequence of the loss of the 
normal protective covering of the pulp, its sensory and perhaps 
vasomotor nerve fibres become stimulated, overstimulated, irritated, 
and then paralyzed by thermal stimuli in the progress of caries. The 
bloodvessels, which retained their tone up to a certain point, suffer 
vasomotor irritation; next, paralysis leading to their dilatation and 
to the throbbing pain. Later, even change of posture is sufficient to 
cause distention of the paralyzed vessels, hence pain in resuming 
the reclining position. Stimulation by cold, until the later stages, 
causes a sharp, continuous pain, ascribed to the paroxysmal con- 
traction of the vessels. In the stages of paralysis heat causes further 
distention of the vessels, and, if gases be present, causes their expan- 
sion with pressure upon nerve filaments. 

The decreasing and delayed response to thermal stimuli must be 
referred to three sources: (1) An increase in the non-conducting 
covering of the pulp — i. e., a lessening of the amount of the fluid 
contents of the dentinal tubuli and a thickening of the dentinal walls, 
which necessarily implies a recession of the pulp from its normal 
position; (2) to degeneration of the sensory nerve fibers themselves; 
and (3) changes in the w T alls of or about the bloodvessels, which check 
vasomotor response and changes in the caliber of the vessels. These 
three classes of reactions still further emphasize the division of the 
pulp diseases into two types, the acute and chronic; the first class of 
reaction is associated with the acute destructive diseases; the second, 
with the chronic constructive but degenerative conditions. 

CONSTRUCTIVE DISEASES OF THE DENTAL PULP. 

The constructive diseases of the dental pulp include all the sec- 
ondary dentin formations, tubular calcification, the formation of pulp 
nodules and calcareous degeneration of the pulp. 

Tubular Calcification. — Definition. — By tubular calcification, or, 
to express the condition more accurately, tubular dentinification, is 
meant the change that occurs in the dentin which leads to an obliter- 
ation of the dentinal tubuli by deposition of dentinal material along 
the inside of the walls of the tubules, with a corresponding atrophy 
of the fibrils. It is a sclerosis of dentin analogous to osteosclerosis. 

Causes and Occurrence. — The apparent cause is a mild degree of 
irritation, not passing the stage inducing constructive metamorphosis, 
and apparently caused by direct irritation of the fibrils, more par- 
ticularly through the action of thermal shock, brushing, mastication, 
29 



450 CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

or action of acids. It occurs in the course of mechanical abrasion 
and erosion of the teeth, under metallic fillings, and probably a 
modification of the process precedes the slow invasion of dental 
caries. It begins at once the enamel is removed from the dentin at 
any point, and the dentin subjected to irritation, showing it to be 
due. to a stimulation of the whole odontoblastic cell (including its 
fibrillar prolongation). It occurs in some degree as a normal vital 
change due to age, and is common in persons who are victims of the 
gouty or rheumatic diathesis. It also occurs in pyorrhetic teeth as 
a result of pulp stimulation (Figs. 304, 353, c, and 397). 

Pathology. — The fibril is lessened in diameter as the lumen of the 
tubule becomes smaller. There is sometimes an increased, but more 
often a lessened, sensitivity of the dentin. 

Other phases of the condition are discussed under transparency of 
the dentin, to which the disease corresponds. (See p. 380.) 

The altered dentin becomes translucent, acquiring a horn-like 
appearance, and, usually, secondary dentin formation begins coinci- 
dently with it. Andrews claims that granules of calcific matter are 
pushed into the fibrillse by the odontoblasts and deposited along the 
inner wall of the tubule, even to obliteration of them. These gran- 
ules give the color to abraded dentin in the region of the pulp cavity. 

Tubular calcification is, for the most part, to be regarded in the 
light of an effect due to a physiological process. It may be regarded as 
a physiological barrier erected against the progress of caries, erosion, 
or abrasion, threatening the invasion of the pulp. While it delays 
the disintegration of the tissue, it does not prevent it. In the cases 
due to age or the irritants produced by goutiness, it is probably 
a local expression of a general sclerotic change, the intercellular 
substance (tubule wall) being formed at the expense of the cellular 
(fibrilla). In senility the change in the dentin may cause the teeth 
to be almost transparent. It requires no treatment. 

Secondary Dentin. — Definition. — By secondary dentin is meant a 
deposit of dentin upon the wall of the pulp chamber, as the result 
of pulp stimulation after the pulp has enjoyed a physiological period 
of rest from dentin formation. It is always attached to the dentin. 

Causes. — The cause of formation of secondary dentin is a stimula- 
tion of the pulp to increased functional activity. This stimulus 
may be provided by any constant irritation of the dentinal fibrils, 
as, for example, when exposed at necks of teeth, upon abraded or 
eroded surfaces, or within cavities of decay. The presence of metallic 
fillings, conductive of thermal changes, may provide the necessary 
stimulus. Gold crowns upon ground-down crowns of vital teeth have 
a similar effect. The slightly irritative effects of oxychlorid of zinc 



SECONDARY DENTIN 



451 



often produce much secondary dentin. It is associated with tubular 
calcification. A pulp capping may provide the stimulus and new 
dentin fill the orifice of exposure. Absolute exposure without treat- 



Fig. 390 



Fig. 392 




Secondary dentin 
formed after exposure 
of pulp by fracture 
during extraction. 

(Tomes.) 

Fig. 391 




Bicuspid in which a 
formation of second- 
ary dentin has failed 
to obviate perforation 
of the pulp cavity by 
resorption. (Tomes.) 




Harding's case of united fracture. The uniting material 
is of coarse osseous structure with numerous lacunal spaces. 
(Tomes.) 



rnent has been recorded as productive of sec- FlG - 393 

ondary dentin. In two cases described by 
Charles Tomes, pulps widely exposed by frac- 
ture of crowns during extraction covered them- 
selves completely in. The histological record, 
as seen in the photomicrograph, demonstrated 
that a plastic exudate was first exuded, which 
later calcified as an amorphous mass. 

Next an irregular lamina was formed, and 
lastly, dentin containing tubules. It is to be 
inferred that both the pulp and its odonto- 
blasts may take part in the process (Fig. 
390). 

I have seen one case in which a wide exposure had been covered in 
sufficiently to enable me to gently indent the covering, which was 




Elastic layer of 
calcific material formed 
over an exposed pulp. 
(From a case.) 



452 CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

convex, with a ball burnisher. Upon removal of the instrument it 
resumed its original shape, owing to its elasticity. The periphery of 
the original exposure was clearly defined (Fig. 393). In another case 
of known exposure with bleeding the patient kept eugenol on cotton 
in the cavity. After several w T eeks the exposure could not be again 
discovered. Age seems to be a cause of general secondary dentin 
formation, but no doubt certain forms of irritation are introduced 



Fig. 394 




Fig. 394. — Secondary dentin filling the pulp chamber is a case of abrasion of a 
cuspid tooth: a, portion lost by abrasion; c, abraded surface; d, secondary dentin, 
filling a portion of the pulp chamber, and acting as a protection to the pulp; e, slender 
point of the pulp — irregular deposits are seen on the walls of the pulp chamber, as at 
/; g, cylindrical calcifications in the root portion of the pulp chamber. 

Fig. 395. — Secondary dentin from the same specimen as Fig. 394, magnified suffi- 
ciently to show the difference in primary and secondary tissue: a, abraded surface 
crown; b, secondary dentin; c, primary dentin; d, junction of primary with secondary 
dentin; e, remains of pulp tissue; /, small oval masses of calcific material. (Black.) 



competent to produce the changes; for example, slight looseness of 
teeth, causing a constant pulp stimulation. At times reflex irrita- 
tion seems to be a competent cause, as in cases of partial abrasion 
the unworn teeth may be affected in equal degree with the worn 
ones. 

It is also true that any form of chronic irritation of the pericemen- 
tum of a tooth may produce arterial hyperemia of a pulp which will 
lead to the formation of secondary dentin or pulp nodule or both. 



SECONDARY DENTIN 



453 



Non-occlusion, mal-occlusion, pyorrhea alveolaris are typical ex- 
amples of the non-septic and septic classes of irritation. (See p. 469). 
Pathology and Morbid Anatomy. — The formation is usually noted 
opposite to some area of injury, and may be distinguished from 
normal dentin by its translucency, or sometimes by its color, which 
may be a light brown. The deposit may be of fairly regular or 
irregular distribution, and even tumors attached to the dentin have 
been described (Fig. 396). 

Fig. 396 





Dentinal tumor within pulp chamber: A, diagram of the tooth, with dotted line 
showing the position of the section B. In B the pulp chamber is shown in section, 
nearly natural size, showing the tumor within. C is an illustration of the tissue of the 
tumor; a, a, the primary dentin; b, irregular tubules connecting the newgrowth with 
the primary dentin — most of these are very dark and irregular; c, c, a calcospherite 
included in the mass; d, apparently a bloodvessel calcified; e, calcified tissue; /, a 
finely granular mass; g, a spur of very transparent dentin. Dentinal tubules appear 
at h, h. (Black.) 



Black has shown that in the deposits against normal dentin the 
first-formed portion contains an almost normal number of tubules, 
but their direction is sharply changed. As the deposits become 
thicker the tubules become fewer, and finally the dentin becomes 
amorphous in character (Fig. 399.) 

Black relates these appearances with the gradual atrophy and dis- 
appearance of the odontoblasts. As the pulp becomes smaller it 
also necessarily undergoes atrophy. 



454 CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

Hopewell-Smith, 1 treating of secondary dentin under the title of 
" Ad ventitious Dentin," mentions several varieties: (1) Fibrillar, or 
that containing tube-like markings finer and less regular than in 
normal dentin. This would correspond to that in Fig. 396, h. (2) 
Areolar, that containing interglobular spaces formed by the non- 
union of calcospherites. (3) Cellular, in which the cells of the 
pulp remain encapsulated in the calcifying matrix. (Fig. 400.) 

(4) Laminar, in which laminated spherites appear (Fig. 396, c). 

(5) Hyalin, having a granular or ground-glass-like appearance (the 
amorphous substance of Black) (Fig. 396,/). He regards the adven- 
titious dentin as formed by pulp cells rather than by the odontoblasts. 
In these cases the pulp deposits calcoglobulin against the dentin. 



Fig. 398 





Fig. 397. — Illustration of the narrowing of the pulp chamber in a molar (superior) 
by the deposit of secondary dentin resulting from abrasion, showing the portions of the 
chamber in which the deposit usually occurs. The light-shaded portion (6) shows the 
original dimensions of the chamber, which, in this instance, seems to have been pretty 
large; a, a point of deep abrasion; c, c, remaining pulp chamber, which is mostly 
filled with irregular masses; d, one of the root canals. It will be observed that the 
narrowing of the root canal is within the original pulp chamber. (Black.) 

Fig. 398. — P.D., primary dentin; S.D., secondary dentin; P, pulp chamber; D, D, 
nodules. 



Apparently in some of Black's cases the calcoglobulin was deposited 
about preexisting fibrillse which continued to persist in the new 
formation, the remaining odontoblasts receding, while in Tomes' 
cases the pulps were compelled to calcify a plastic exudate as a sort 
of basis for the beginning of tubule formation. This is probably the 
case in formation of secondary dentin as a repair of exposure under 
a cap. Black has shown that in abrasion the deposit is more regular 
than in caries, without doubt due to the fact that the thermal irrita- 
tion in caries is more irregular than the irritation of the fibrillar by 



Histology and Patho-Histology of the Teeth. 



SECONDARY DENTIN 455 

abrasion. A deposit projecting from any point about the pulp cavity 
side into the pulp is called a "dentinal tumor" (Fig. 396). 

The entire crown may be removed by abrasion and yet the pulp 
be protected. In some cases the protective action ceases and the 
pulp becomes closely approached or exposed (Fig. 280), probably 
due to a cessation of secondary dentin formation, the result of 
degeneration and loss of odontoblasts, or it may be due to very 
rapid wear (a later stage of Fig. 395). 

The mode of deposition upon the sides of the canal in abrasion, 
shown by Fig. 394, is quite characteristic, and sometimes annoying 
in that it permits an unlooked-for exposure, which, upon cocain 
anesthesia, causes one to follow a fine opening for an eighth of an 
inch or more before finding a proper canal. 

Deposits in canals may occur, lessening their lumen and increasing 
the difficulty of canal exploration (Fig. 398). 

"Secondary growths in cases of abrasion are not confined alone to 
the abraded teeth, but other teeth which have escaped wear may be 
affected in equal degree. In all of these cases there is direct evidence 
that the odontoblastic layer has been stimulated to increased 
activity and produced the regular secondary deposition." 1 (See 
Reflex Hyperemia of the Pulp, p. 470) . 

Secondary dentin is often accompanied by other constructive 
changes in the pulp — i. e., pulp nodules and calcareous degeneration 
(Figs. 398 and 404). 

Miller has shown that dentin resorption by the pulp may be 
repaired by a new deposit of secondary dentin, which Hopewell- 
Smith has shown to be of the nature of cementum. (Fig. 422.) 

Tomes 2 describes and illustrates a peculiar case of united fracture 
occurring in the practice of Mr. Harding. In an incisor an oblique 
fracture occurred which entirely separated the fractured segment, 
yet a plastic exudate occurred which, when calcified, attached it to 
the fixed portion of the tooth. The new formation did not resemble 
dentin (Fig. 392). 

Fig. 309 illustrates a case of repair of an incisor fractured at a 
point well up beneath the gum, a condition reasonably insuring 
asepsis. A firm reattachment occurred. I have seen such a fracture 
which resulted in pulp death and the coronal portion remained in 
situ for two years (according to the patient). This would give time 
for such a plastic exudate to form. In another case I was compelled 
to remove a pulp for hyperemia two months after a fall fractured a 
tooth in this location (see p. 324). 

1 Black: American System of Dentistry, vol. i. 2 Dental Surgery. 



456 CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

Kirk 1 records a case of immediate replantation in early life, followed 
in old age by root resorption. The tooth, when extracted, contained 
secondary dentin, which could only have formed as the result of a 
reattachment of the pulp. 

W. H. Trueman 2 reported that hypersensitive dentin was noted 
some years after a replantation under similar conditions. 

Fig. 399 




Calcification or deposit of secondary dentin, resulting from caries of an incisor: 
A, diagram of section of incisor, showing caries at a, and secondary dentin at b. B, 
illustration magnified 200 diameters, to show the tissue of the secondary dentin: a, 
pulp chamber; b, b, secondary dentin; c, primary dentin. It will be noticed that the 
dentinal tubes in the secondary dentin gradually disappear, giving place to a clear 
calcification. (Black.) 



Osteodentin. — Tomes states that secondary dentinal deposits may 
assume the character of osteodentin, a form of dentin found in the 
teeth of some animals, in which the tissue presents combined char- 
acteristics of both bone and dentin. He cites the example also that 
elephants' tusks are frequently repaired with osteodentin after injury. 
The specimen illustrated (Fig. 400) was taken from a case in which 
the coronal portion of the pulp chamber was almost obliterated by 
a deposit of secondary dentin. Probably some of the pulp cells 
have taken on the characteristics of osteoblasts. Tissue resembling 
cementum seems to be frequently found as a tissue of repair (Fig. 400) . 



Proceedings of the Academy of Stomatology, 1902. 



2 Ibid. 



ShJCOXDAHY DHNTIN 



457 



Results of Secondary Dentin. — The formation of large masses of 
secondary dentin unquestionably brings about a degenerative con- 
dition of the pnlp which may become a cause of neuralgia. The pulp 
may die, and, becoming infected, may produce pericemental irrita- 
tion. In one case seen the secondary deposit in the pulp chamber 
had separated the canal filaments of the pulp of a multirooted tooth 
into independent pulps, one of which was dead and the others alive 
and undergoing degeneration. The specific symptoms were those of 
pericementitis — i. e., elongation and tenderness to percussion. 

In another case of a first upper bicuspid the lingual filament was 
perfectly covered in and vital. The buccal filament, likewise enclosed 
and isolated, contained an abscess within the pulp. 

The symptoms complained of, however, were those of acute peri- 
cemental irritation, simulating incipient septic apical pericementitis 
(Fig. 432). 

Fig. 400 




Osteodentin: A, outline of incisor, showing a narrowing of the root canal at b by 
a deposit of osteodentin. B, illustration of the tissue: a, primary dentin; b, line of the 
beginning of a growth of secondary dentin; c, secondary dentin; d, layer of granular 
matter; e, osteodentin; this has the lacunae at g and dentinal tubes at k; /seems to be 
the surface of the osseous deposit; i, irregular crystalline deposits; h, the pulp chamber. 
X 350. (Black.) (Tomes.) 



It has been shown by Hopewell-Smith that microorganisms may 
enter the pulp by way of the spaces or tubes in adventitious dentin. 
In Burchard's case a molar containing a deep cavity filled with zinc 
phosphate gave vague pain, finally referred to the tooth, which 
'responded only faintly to hot applications and not at all to cold ones. 
Secondary dentin was found complicated by calcareous degeneration 
— i. e., a degenerated pulp was present. 



458 CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

In certain cases a deposit extends well into a canal, totally obliter- 
ating it for much of its length. Unless symptoms be present it may 
ordinarily be left. In such cases thermal tests for pulp vitality seem 
often inconclusive. The electric current should be a more satisfac- 
tory means of diagnosis, provided the dentin be moist. Secondary 
dentin is sometimes quite hypersensitive, as shown by attempts at 
entering the pulp; in most cases it is quite insensitive until the pulp 
is reached. It is also difficult, as a rule, to force cocain through 
secondary dentin, even with a compound syringe, and arsenic acts 
slowly, though it devitalizes if the dentin be sensitive. (See Dry 
Gangrene, p. 562, also p. 424.) 

Treatment. — Secondary dentin which has been regularly deposited, 
and particularly in the canals of anterior teeth, calls for no treatment. 
Should, however, great hypersensitivity of the dentin and pulp, or 
pulp disease, be evident or inferred from symptoms, the pulp should 
be removed. Canal opening may involve a search of some difficulty 
and necessitate the removal of much dentin. The canals may be 
much constricted, especially at that portion nearest the pulp cham- 
ber. The condition may be more or less complicated by the presence 
of pulp nodules or calcific degenerations in addition to the secondary 
dentin. 

Pulp Nodules. — Definition. — Pulp nodules (pulp stones, nodular 
calcifications) are masses of more or less translucent, calcific material, 
apparently the result of secretion, having a fairly definite histological 
structure differing from that of dentin, and occupying a position 
within the pulp substance. They are rarely fused with the dentinal 
walls of the pulp chamber, and then are included by formation of 
secondary dentin about them. 

Occurrence. — While these growths may occupy the pulp chambers 
of teeth in which the pulp has been the seat of direct irritation, their 
occurrence is by no means confined to such teeth. They are found not 
only in teeth which have suffered abrasion, erosin, and slowly pro- 
gressing caries, but, as pointed out by Black, they may, and frequently 
do, form in other teeth of the same denture which are not directly 
involved in the irritation. This investigator notes that irritation of 
the pulp of one tooth of a denture very frequently causes a general 
hyperesthesia (due to mild reflex hyperemia) of the pulps of all of 
the teeth. Pyorrhea producing tooth movement or apical peri- 
cemental irritation can produce arterial hyperemia of the pulp and 
thereby pulp nodules. This is due to the constructive effect of mild 
hyperemia. 

Nodules and secondary dentin or pulp hyperemia may occur in 
sound teeth ground for crowns. This simply indicates a necessity 



PULP NODULES 



459 



for antisepsis in the cement, or a non-conductor as varnish, or chloro- 
percha over the teeth before cementation. The conditions are not 
unlike those in a cavity of simple depth and to the mind of the 
writer do not necessitate devitalization before crowning, as many 
live for years. Nodules are found much more frequently in the teeth 

Fig. 401 




PN 



A pulp nodule fused to the parietes of a pulp cavity. Prepared by grinding: PN, 
pulp nodule; D, dentin of the tooth. X 15. From section by J. F. Colyer. (Hopewell- 
Smith.) 



of middle-aged persons than in those of youth, although they may 
be present as early as the ninth year, as shown by skiagraphy. They 
, occur more frequently multiple than single. Some of the larger 
nodules are evidently formed by the coalescence of smaller ones. 

Pathology and Morbid Anatomy. — The structure of pulp nodules 
does not resemble that of dentin; they possess about the same degree 



460 CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

of translucency and hardness as secondary dentin. Outwardly they 
may assume almost any form; they range in size from minute bodies 
to a size sufficient to almost obliterate the pulp (Figs. 398 and 404). 

Fig. 402 




Section of a pulp nodule, showing many calcospherites, as pointed out by a. a. (Black.) 

A section of a nodule exhibits the presence of a number of concen- 
trically laminated bodies, recognizable as hardened calcospherites. 
Black found them to rarely make up any considerable portion of the 
bulk of the nodule. The remainder of the nodule is made up of 
structureless material which may contain a few fine tubes. 

Fig. 403 




Deposit of calcoglobulin within the tisues of an inflamed pulp. (Black.) 

He also found deposits in the pulp which throw light upon the 
possible origin of nodules in some cases, and to some extent upon 
the conditions under which they may be formed. In the pulp of 
a second molar of a girl, aged fifteen years, in which there had been 



PULP SODULES 



461 



decided subjective evidences of pulpitis recurring at intervals for a 
period of two months, he found a mass representing a pulp nodule in 
its soft state. " About one-half of the coronal portion of the pulp was 
involved in the inflammation; lying a little inside of the layer of 
odontoblasts were several masses similar to Fig. 403, having globular 
forms in their mass or attached to their margins. The globular 
bodies present the laminated appearance of calcospherites." These 
masses may in all probability be interpreted as intermediate products 
in the formation of nodules; they have not yet become calcified. 

Fig. 404 




Calcification of the dental pulp: At A is shown the outline of a lower molar with a 
cavity at b. The pulp chamber is much reduced in size and filled with calcific material, 
as shown in B. a, a, large granular mass of calcific material, which is very transparent, 
but finely granular. A very few irregular lines are seen in the centre, which slightly 
resemble dentinal tubes; b, an erratic growth of irregularly formed and unusually 
transparent dentin; c, line of the growth of dentin from the floor of the pulp chamber — 
the growth from other directions is so perfectly regular as to leave no markings; d, 
margin of the cavity of decay; e, a bundle of cylindrical forms of calcific material 
extending down into the root canal. These extended to the apex of the root. (Black.) 



A small nodule may be made up of laminated, structureless 
material, the laminae being arranged about a central nucleus, the 
nature of which is not clear, but may possibly be calcified dead cells 
(Fig. 405). 

« The conditions of calcification of nodules are not definitely known. 
Hopewell-Smith considers that they are deposited by the pulp cells as 
a secretion about themselves, and that the cells are later obliterated 
or may persist in situ (Fig. 406). He also describes and illustrates 



402 CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

a case of a nodule which had within it a pulp cavity containing 
pulp tissue. 

Pulp nodules occur, as a rule, in the better grades of teeth which 
show constructive tendencies upon the part of the pulp. 

Fig. 405 




A pulp nodule isolated from the pulp. Shows its central nuclear formation and 
its concentric lamination. Prepared by grinding. X 50. From collection of G. W. 
Watson. (Hopewell-Smith.) 

It is possible that in these pulps the pulp cells under conditions of 
irritation secrete calcoglobulin, which in part is developed into spher- 
ites and in part remains without definite histological characteristics. 
The masses are probably calcified after their deposition. Whatever 
the origin of the masses — by cell secretion or otherwise — the histo- 
logical record indicates a gradual increase in the size of the deposit. 
Pressure upon the nerves results in irritation and an increase in 
pulp hyperemia which causes the reaction to thermal changes. Pulp 
nodules are usually found in the coronal portion of the pulp, but 
sometimes exist in the root portions, either free or embedded in 
secondary dentin. If they obstruct the lumen of the canal they 
cause interference with the circulation and nerve tissue and may 
produce great pain. Bunting calls attention to the possibility that 
the nodule moving freely in the pulp may allow arterial pressure to 
raise it, permitting blood entrance, while the venous pressure may 
return it to place and prevent exit of blood thus inducing continued 



PULP NODULES 463 

internal pressure in the pulp (a venous hyperemia), thus causing 
functional disturbance and pain. 1 As in the case of secondary dentin, 
nodules may be produced by reflex hyperemia, as they are quite 
frequently found in teeth near to an impacted tooth. 

Symptoms. — Multiple nodules may exist in a dental pulp and give 
rise to no evident symptoms whatever, as is shown by their presence 
in extracted teeth, many of them free from caries, and in which there 
was no history of pain. On the contrary, the pulp of a tooth may 
react persistently to thermal changes or even be the seat of intract- 
able pain without a depth of carious invasion which would lead to 
the inference of acute pulp disease; and relief only be secured 
through devitalization of the pulp, which upon examination may 
reveal a small or large pulp nodule. 

Fig. 406 



PN 




MN 



PN 



MN 



The formation of the pulp nodule. Prepared by Mr. Hopewell-Smith's process. 
PN, pulp nodules; MN, medullated nerve bundles; T, pulp tissue; C, capillary. 
X 230. (Hopewell-Smith.) 

The symptoms attendant upon the presence of nodules, so far as 
they can be made out, appear to be of two types — those associated 
with small and those with extensive deposits. Reflex pain is the 
common associate of both. 

Small Deposits. — While it is true that pulp nodules may some- 
times exist in apparently sound teeth without inducing pain, yet the 

1 Dental Cosmos, February, 1912, p. 169. 



464 CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

pulps of teeth containing them become excessively hyperesthetic 
under what are ordinarily mild sources of irritation. This is mani- 
fested, first, through the contents of the dentinal tubuli; the dentin 
becomes exquisitely sensitive and cool water directed into a shallow 
cavity produces a paroxysmal and excruciatingly painful response 
from the pulp. In the absence of direct, extraneous irritation of the 
pulp, the dental symptoms may be absent, but a persistent neuralgia 
may be located at some distant point. Pain in the ear is a frequent 
symptom. Occasionally an obstinate scalp neuralgia, with the exist- 
ence of a hyperesthetic spot, appears. Pain in the eye, with tender- 
ness over the supra-orbital foramen, is also common. Guilford 1 has 
reported a case of tic douloureux of two years' standing, the result 
of pulp nodules. The pain may be recurrent or persistent. If, in the 
absence of a more probable explanation of the pain, the pulp nodule be 



Fig. 407 



Fig. 408 



Fig. 409 





Pulp nodules in the radicular and 
coronal portions of the canal. (Skia- 
graphs by Price. 2 ) 




First and second bicuspid roots 
filled. Pulp nodule in first molar. 
(Skiagraph by Lodge.) 



suspected, and arsenical applications be made to devitalize the pulp, 
it is found that not only is intense pain caused, but examination after 
even a week or more shows the pulp to be still vital and hypersensi- 
tive; and, in order to effect its destruction, repeated applications 
and large doses of arsenic must be used. Cocain introduced by 
cataphoresis is also apt to be slow in action. 

Large Deposits. — In extensive deposits of pulp nodules the 
dentin may be almost devoid of sensation, and applications of heat 
or cold, even in large cavities, may be followed by delayed and faint 
pulp response. Such cases, however, commonly give a history of 
reflex neuralgia and vague dental pains extending over a period, it 
may be, of years. With some large deposit the pain may be exquisite. 

Diagnosis. — Their diagnosis by means of the .r-rays is positive 
(Figs. 407, 408, and 409), but their diagnosis by symptoms may only 



1 Private Communication. 



Items of Interest, 1901. 



CALCIFIC DEGENERATION OF THE PULP 465 

be inferential and confirmation be lacking until after devitalization 
of the pulp and the finding of the pulp nodules in its substance. 

The tardy action of arsenic is also observed in the cases of large 
deposit, it being frequently necessary to devitalize the pulp piece- 
meal, and sometimes the arsenic will hardly be tolerated at all. 

Treatment. — Pulps inferred or shown by .T-rays to contain nodules 
should be removed. The cataphoric apparatus or compound syringe 
or even ordinary cocain pressure may be used to benumb the pulp 
by cocain; at least, sufficiently for the removal of the nodule. If 
desired, the remainder of the pulp may generally but not always be 
anesthetized by the same means and removed. The bloodletting 
attendant upon removal of the bulb of the pulp usually permits an 
arsenical application for devitalization of the remainder of the pulp 
to be painlessly made, but this is not always the case. 

The same result may be attained by drilling open the pulp cavity 
while the patient is under the influence of nitrous oxid gas or somno- 
form, or, possibly, intra-alveolar injection of cocain. 

At times arsenic may be applied to the pulpal wall of the cavity, 
if one exist, or in a specially prepared pocket, without production 
of painful reaction. 

After forty-eight hours a portion of dentin is to be removed and 
a stronger application made. When the pulp is closely approached, 
the arsenic is to be left a week or longer in position, when, as a rule, 
the nodule may be removed. Another application may then be left 
in position for a week or longer to insure devitalization. 

If, after devitalization, the nodule or calcific degeneration be 
found as a spicular deposit in the mouth of the canal, it may usually 
be removed by teasing it from side to side, first soaking the part 
with a sodium dioxid solution, or 50 per cent, sulphuric acid, which 
quickly destroys the organic matter of the pulp. 

Pericemental reactions are quite apt to follow the removal of such 
pulps. This result is best obviated by awaiting the thorough death 
of the pulp filaments before attempting their removal. 

If such reaction arise, strong sedatives, such as menthol solutions, 
are to be applied on cotton as root-canal dressings, and counter- 
irritants are to be applied to the gum. (See Xon-septic Apical Peri- 
cementitis.) 

Calcific Degeneration of the Pulp. — By calcific degeneration is 
meant the infiltration of inorganic matter derived from the lymph 
into tissue which is dead or undergoing degeneration. It occurs in 
any part of the body in which the necessary conditions are present. 
(See p. 87.) 

Cause and Pathology. — The conditions apparently necessary for 
the production of calcific degeneration are those which occur in a 
30 



466 CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

semistagnant blood current. An acid reaction occurs owing to the 
presence of an excess of carbon dioxid, which favors deposition of 
inorganic matter. The albuminous matter of the tissue undergoes 
degenerative changes owing to the faulty nutritive supply and waste 
removal. 

Probably some cells die. They or their constituents have some 
affinity for inorganic salts which are taken up from the lymph. Thus 
gradually the tissue becomes infiltrated. 

Those causes which produce a sufficient degeneration of pulp tissue 
to induce the above process are: (1) The pulp exhaustion due to 
the formation of secondary dentin or pulp nodules; (2) continued 
hyperemia or chronic inflammation in which venous hyperemia plays 
a part. 

Fig. 410 




A, outline of a lower molar, with a large carious cavity at a; b, pulp chamber; 
the shaded portion, c, was occupied by cylindrical calcifications. B, cylindrical 
calcifications. X 100. (Black.) 



Pathology and Morbid Anatomy. — The calcific material, unlike the 
cases of nodular calcification, encloses the anatomical elements of a 
pulp in process of degeneration in a mass produced by deposition, 
not secretion. In the root portions of pulps in which fibrous ele- 
ments have become pronounced the calcification may be tubular or 
cylindrical in character, the nature of the calcareous masses being 
apparently a deposition about and along the fibers (Fig. 410). 

The pulps are, of course, living. There is a comparative absence 
of cellular elements in the pulp — i. e., they have atrophied, degen- 
erated, and been absorbed. Upon optical examination the masses 
are seen to be opaque, are brittle, and decidedly unlike pulp nodules 
in form. 

Another evidence of the cellular degeneration is seen in the great 
ease with which such pulps are removed after devitalization, even 
the most minute apical portions freely coming away after slightly 
catching a hook in the pulp — i. e., the usual odontoblastic 




CALCIFIC DEGENERATION OF THE PULP 467 

attachment to the dentin is not present. When extracted these pulps 
have a granular feel to the fingers, and when dry may be quite stiff 
(Fig. 411). 

Symptoms. — Degenerations of the pulp, as a rule, present symptoms 
of reflex pain, vaguely referred to other parts. The response to hot 
applications is usually greater than that to 
cold ones, and both are delayed — i. e., five FlG - 4U 

seconds or more may elapse before pain 
follows a severe test like the intensely cold 
spray of ethyl chlorid or a hot burnisher or 
blast of hot air. At times with an open 
pulp chamber the symptoms of chronic 
pulp inflammation are obtained. There 
may be a painful reaction to arsenic applied 

to the pulp. Lingual filament of pulp 

" ^' of an upper molar, broken 

Diagnosis and Treatment. — ihe.r-rays may in extraction. The rigidity 
afford a positive diagnosis, but in their ab- °[ the filament ™ due to 

. ,. ° . the presence of calcific 

sence the diagnosis, apart from the inference granules. 

from the symptoms, is a postmortem one. 

In cases warranting the interference, in which there is a delayed 

response to intense thermal tests applied to a filling or a clean 

pulpal wall, the dentin over the pulp should be removed and the 

pulp devitalized. Upon removal of the pulp it may be found to 

contain one or more large or many granular masses. 

Fig. 411 illustrates a case discovered upon fracture of a molar 
during the operation of extraction. In another case the pulp was 
slightly- bendable when extracted, but after drying for a half-hour 
became at its apical end of needle-like sharpness and stiffness. It 
was filled with calcific granules. 

The constructive diseases of the pulp are an evidence of an attempt 
upon the part of the pulp to protect itself; but with the exception, 
perhaps, of a very regularly deposited secondary dentin the effects 
react upon the pulp itself, causing its destruction. To what extent, 
therefore, secondary dentin is beneficial is an open question. 

Evidences of constructive action upon the part of the pulp may 
occasionally be noted in the temporary teeth — e. g., secondary dentin 
following deep abrasion. 

There do not seem to be any observations as to the formation of 
nodules or calcific degenerations in the pulps of temporary teeth, but 
there is no good reason why they should not occur, particularly after 
abrasion. The pulp diseases of the temporary teeth are usually of 
an acutely destructive nature, which may account in some degree 
for the absence of reports touching this subject. 



CHAPTER XVI. 

DESTRUCTIVE DISEASES OF THE DENTAL PULP. 

This class of pulp diseases consists of those of an acute character, 
although chronic diseases may arise as sequels of the original con- 
ditions. They are essentially destructive in character and attended 
by prompt degeneration of pulp tissues. The most important, 
clinically, are those having an evident association with disorders 
of the bloodvessels of the pulp. 

HYPEREMIA OF THE PULP. 

Hyperemia of the pulp is an excess of blood in the more or less 
dilated vessels of that organ. It is of two forms: active or arterial 
hyperemia, and venous or passive hyperemia or congestion. These 
two classes differ in their probable direct causations and in effects. 

Arterial Hyperemia of the Pulp. — Definition. — Active or arterial 
hyperemia of the pulp is an excess of blood in the dilated arteries 
and capillaries of the pulp, the pulp functions being increased in 
mild continued cases or disturbed by a gradual passage of the con- 
dition into a venous hyperemia in more severe cases. 

Direct Causes {Thermal Shock). — The most common cause of active 
hyperemia of the pulp is a lessening of the non-conducting covering 
of the organ, enamel, and dentin, leading to either (1) direct pulp 
shock through the chilling or heating of dentin by thermal changes, 
or (2) by direct fibril irritation which through the odontoblasts and 
their neural connection invites, by vasomotor stimulation, a flow of 
blood. This increases the functions of the pulp and therefore its 
irritability and response either as pain or as further hyperemia or 
both. With a deep metal filling present the first explanation serves. 
With a shallow metal filling the second fits the fact of slow onset of 
hyperemia, recognizable by pain to cold. It is surprising to what 
an extent the pulp may protect itself against thermal stimuli by the 
formation of secondary dentin and tubular calcification. Thus 
teeth filled with metal alone often produce a pulp hyperemia, of which 
the patient complains as painful reaction to cold, but which passes 
away in a few weeks. When the cavity is of moderate depth the 
bruising of fibrils by filling and the thermal shock to fibrils are 
(468) 



HYPEREMIA OF THE PULP 



469 



causes acting through fibril stimulation. The vigorous use of sand- 
paper disks in finishing large fillings may precipitate an attack of 
pulp hyperemia, but only if the pulp is in a critical condition. The 
loss of tooth substance mentioned may occur either through abrasion, 
erosion, fracture, or caries. The condition frequently occurs without 
direct exposure of the dental pulp, and at times when cavities are 
relatively shallow. Even the simple cervical exposure of dentinal 
fibrils may cause it, but does not often do so. (See explanation 2.) 



Fig. 412 



Fig. 413 



Fig. 414 



Fig. 415 




Fig. 412. — A, Cavity or metal filling approaching pulp: B, hyperemic (sometimes 
inflamed) pulp; C, area of hyperemia of apical tissue, due to extension from the pulp 
or possibly to back pressure of blood. 

Fig. 413. — A, Area of non-septic inflammation of apical tissue due to injury as 
from a blow or malocclusion; B, hyperemia or mild non-septic inflammation of the 
pulp due to overflow from the apical tissue. 

Fig. 414. — A, pyorrhea pocket; septic inflammation at C; B, area of lesser inflam- 
mation (non-septic); D, hyperemia of pulp; E, normal tissue. 

Fig. 415. — A, ulcerated or necrotic alveolar wall due to injury and infection; B, 
inflammation more or less non-septic (lesser inflammation) ; C, hyperemia of pulp 
due to overflow of blood at B. An abscess on an adjoining root has the same pathology. 
If extending to the molar it infects its pulp from the apex. (See pages on Areas.) 



Irritation of Fibrils by Sepsis. — Septic dentin beneath fillings acts 
as a cause by constantly irritating the dentinal fibrils. The leaving 
of septic dentin in a cavity and a leaking rilling over sound dentin may 
so act. Inclusion of saliva beneath a metal or gutta-percha filling, 
and the imperceptible shifting of a filling during placement, are 
causes of septic dentin. Amalgam may so shift if slight yet excessive 
force be used in finishing at the first sitting. The sign is the appear- 
ance and disappearance of moisture at a visible margin as the filling 
is moved. This is often unobserved unless one be very thoughtful 
of its possibility. The cement beneath an ill-fitted crown also ap- 
pears to become saturated with saliva or serum, and its odor indi- 
cates septic irritation. This is less likely to occur under gutta- 
percha, but odor can be noted in some such cases. This may be 
the real cause of death of pulp in ground sound teeth and calls for 
avoidance by the use of thymol in the cement. Acute hyperemia 



470 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

may occur from the presence of a pulp nodule, probably also a result 
of mild hyperemia produced by some other cause. 

Associated Hyperemia of Pericementum. — All pulp hyperemias, if 
intense, may extend into the apical tissue and cause pericemental 
hyperemia with symptoms of tenderness to touch (Fig. 412). 

Indirect Causes. — Extension of Inflammatory Area. — Pulp hyper- 
emia may also be caused by injury or disease of the apical tissue of 
a tooth containing a vital pulp. Malocclusion from any cause, 
overfull fillings or crowns, a blow, or overmalleting, or the extrusion 
occurring in pyorrhea alveolaris, is competent to produce an apical 
hyperemia or inflammation which extends into the pulp (Fig. 413). 
An abscess upon an adjacent tooth may have its area of hyperemia 
extend into the apical tissue of the tooth adjoining, thus producing 
hyperemia of the pulp (p. 135, Fig. 415). A fairly deep pyorrhea 
pocket may frequently act in a similar manner, the inflammation 
extending as a non-septic one up to the apical tissue (Fig. 414). 

Reflex Action. — An intense hyperemia in the pulp of one tooth 
may, by reflex action, produce hyperemia, with its characteristic 
response to hot and cold applications, in another tooth. In a typical 
case an inflamed apical half of the pulp of a third molar produced 
a hyperemia in the pulp of the first bicuspid which subsided upon 
removal of the cause in the molar. Any of the causes exciting hyper- 
cementosis (being causes of pericemental hyperemia) may produce 
pulp hyperemia, the apical constriction being an added complica- 
tion. An aphthous ulcer upon the gum over a tooth has produced 
arterial hyperemia of the pulp by reflex or by extension of the area 
of lesser inflammation which may in some cases extend a half inch 
or more. Also an ulcerated alveolar process resulting from infected 
alveolus, or the use of alveolar forceps, or even the regular healing 
of an alveolus after extraction, may cause it in a healthy adjoining 
tooth by extension of the area of inflammation or even in a distant 
tooth by reflex. Also any irritation along any branch of the fifth 
nerve or any of its terminals may reflexly induce a hyperemia of 
the pulp (Fig. 415). A common cold by irritating the terminals 
of the fifth nerve has produced it, as may a tumor. 

Unquestionably, systemic conditions, as malaria, or syphilis, or 
irritation in another part of the body than that supplied by the fifth 
nerve, as the uterus or bladder, may excite reflex pain in the teeth, 
which, if repeated, sooner or later excites a hyperemia, as in the case 
of scalp tenderness from dental disease, and which will probably be 
temporary. The mode of hyperemia production is probably a dila- 
tation of bloodvessels due to vasomotor disturbance produced by 
reflex action. 



I 



HYPEREMIA OF THE PUlP 471 

Apart from the hyperemia occurring in inflammation and that due 
to septic dentin, or a septic extradental inflammation, it may be 
said that arterial and venous hyperemia are mainly due to non- 
septic causes, and even in septic cases to be mainly in itself aseptic, 
in so far as the pulp is concerned. For this reason if the cause can 
be removed and the pulp sedated (when necessary) prognosis for 
pulp conservation is favorable, certainly in mild cases in which the 
pulp is not directly exposed by caries. 

Idiopathic Hyperemia. — In some cases with sound teeth no obvious 
cause can be found, perhaps the case is one due to infarctions 
(which see) or pulp nodule. The latter can be located by skia- 
graphy. Lower incisors are especially prone to it. 

Symptoms. — The symptoms of arterial hyperemia vary according 
to the degree of vascular disturbance. So long as a quick, sharp 
pain is produced by contact with cold or hot substances, ceasing 
immediately, and only reappearing in response to direct stimuli, no 
serious vasculaT disturbance is inferred; but w T hen paroxysms of 
sharp pain, lasting from many minutes to hours, follow upon an 
application of cold to a carious cavity, an unbroken enamel surface, 
a filling, or an area of erosion or abrasion, a profound disturbance of 
the vessels of the pulp is indicated. 

The pains, in the absence of direct irritation, are, as a rule, but 
vaguely located. During paroxysms it is of a lancinating character, 
and usually reflected to another part than the tooth affected — e. g., 
a sound tooth at a distance, the gum between or above the teeth, the 
ear, the eye, the supra-orbital region, the infra-orbital region, the 
scalp,, the chin, the arm, etc. 

As a rule, when an upper tooth is affected, the pain is located in 
the superior maxillary division of the fifth nerve; if a lower, in the 
inferior maxillary division. The pain varies in intensity from a vague 
uneasiness to an acute neuralgic attack, with tender spots over the 
point of emergence of the nerve tracts, as at the supra-orbital and 
infra-orbital and mental foramina. The neuralgic pains are not 
always constant; they may disappear from the second or third 
division of the fifth nerve and appear in the first. 

The proof of the direct connection between the pulp pain and the 
neuralgia may, in some cases, be clearly made out by the thermal 
test. When a jet of cool water is directed against the tooth whose 
pulp is affected, it may produce, in addition to a local pain, an 
t aggravation of the neuralgic pains, but one must carefully exclude 
the extradental causes before diagnosticating a necessity for inter- 
ference with the tooth tested. 



472 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

Pathology and Morbid Anatomy. — The one distinctive and charac- 
teristic anatomical condition associated with active hyperemia is an 
irregular dilatation of the vessels of the pulp. 1 Fig. 416 represents 
a section of the pulp of a tooth extracted during a paroxysm of 
acute pain — "acute paroxysms of pain lasting for an hour or more 
were occasionally occurring in consequence of very trivial changes 
of temperature; the condition had existed for several weeks." In 
some cases of a similar character — i. e., presenting the same symp- 
toms, but extracted during an interval of quiet — nothing remark- 
able is presented. The gradual enlargement of the veins indicates 
the lessening outlet at the apical foramen; or, in other words, the 
beginning and establishment of a venous hyperemia. 

The most rational explanation of the dilatation of the vessels is 
that it is an irregular paralysis of vessel walls — i. e., of vasomotor 
nerves. Whether the more usual painful responses of the pulp to 
thermal stimuli are due to the stimulation of vasodilator fibres, 
which causes hyperemia, is a matter of doubt, but the pathological 
conditions noted in pronounced hyperemia signify a paralysis of 
vasoconstrictor fibers. Subjected to repeated overstimulation, they 
become inactive and the vessel walls yield to the pressure of the 
blood column. Black's researches indicate that the vessel walls may 
recover their tone and the vasoconstrictor nerves their functional 
activity after paralysis. Certainly, clinical experience shows that 
in all purely arterial hyperemias, or even those associated with mild 
venous hyperemia — for the two may be inseparable — in cases with 
symptoms, the cases can be cured if the causes can be removed. 

When a tooth pulp responds to thermal stimuli, especially to mod- 
erate heat or cold, hyperemia is inferred ; but whether the case is one 
of pure arterial hyperemia, mild or severe, or of venous hyperemia or 
of hyperemia of true inflammation must be decided by the nature 
of the cause acting, the physical condition of the pulp (whether 
exposed or not), the length of time continued, and the length of par- 
oxysm produced. The fact of hyperemia and its location are first 
determined, next a cause is sought and, if direct, is removed or ren- 
dered incapable of action by treatment of the tooth; for example, 
placement of sedatives, intermediates, etc., in cavity cases, either 
without or with filling removed (if previously placed) . Quiet ensuing 
and the pulp not being exposed, arterial hyperemia due to the appro- 
priate direct cause is diagnosed, tentatively at the first sitting — 
positively after partial treatment. This also indicates the final 
treatment. If no explanation of cause be found in the crown of the 

1 Black: American System of Dentistry. 



HYPEREMIA OF THE PULP 



473 



tooth in question, the various indirect causes or reflexes are looked 
for and if one be found it is removed by treatment. If relief 
ensue the tentative diagnosis of hyperemia by extension or reflex 
in the pulp which seemed at fault is confirmed by the therapeutic 
test. 

Fig. 416 
I 




Hyperemia of the dental pulp, showing the injection of the vessels: a, a, mem- 
brana eboris, or layer of odontoblasts; b, b, b, b, vessel distended with blood: c, c, c, c, 
points from which the blood has fallen in handling the section. (Black.) 



If the case be idiopathic and demand relief the pulp should be 
removed and the diagnosis of hyperemia is confirmed, though the 
cause may remain obscure if no nodule is found. In cases of cavity 
with pulp exposure, with possible sepsis and inflammation, or septic 
cases with suppuration, the symptoms noted under such conditions 
are considered. In routine work such pulps are said to be inflamed 
and removed; they may be conserved in special cases of course. 
Any hyperemia present is incidental to the inflammation. 

The £-ray may be of use in clearing the diagnosis in some cases; 
for example, of pulp nodules or abscess on adjoining tooth. 

The grade of severity of hyperemia is determined by the pain 
produced on application of the thermal test. 

The following history of a case offers a good example of hyperemia 
(so diagnosticated). A central was drilled lingually with a round 



474 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

bur, by a dentist who mistook a vital tooth for the one threatening 
an abscess. Finding it vital when the pulp was expose^ at a minute 
orifice, he filled with gold, evidently laying a cylinder of gold across 
the exposure. For two years the pulp reacted to cold, the response 
finally becoming so severe that each effort at cleansing the teeth 
caused pain from thermal shock. As the adjoining tooth was without 
a lingual pit, and the electric light showed a deep filling, it was 
removed, and the condition related found. The attempts to remove 
the pulp by cocain pressure failed four times, once after sedation, 
and repeated applications of arsenic were necessary. 

It is to be remembered that arterial hyperemia may be of several 
grades of severity, according to the vascular disturbance. 

Fig. 417 




Dilated bloodvessels from the dental pulp in hyperemia, from tooth extracted during a 
paroxysm of intense pain. (Black.) 



The temperature of the water used in testing should not be lower 
than 60° F., and it should be applied drop by drop. A normal 
pulp will rarely respond painfully to a few drops of water at the 
temperature named, flowed into a cavity; but a hyperemic pulp will 
almost invariably respond vigorously. As a rule, a current of air 
from a chip blower is a test of sufficient severity. 

In the absence of a carious cavity the source of the pain is to be 
sought in large fillings, testing each tooth by dropping cool water on 
the filling; in cases of erosion or abrasion the test is made upon the 
exposed dentin. The tooth which responds with a quick paroxysm 
of intense pain, passing away slowly, is diagnosticated as the seat of 
pulp hyperemia. 

In making this test doubt may arise as to which of two adjoining 
teeth is at fault. A small square of rubber dam, with a single hole 
punched in its centre, may be passed over the tooth to be tested, thus 



HYPEREMIA OF THE PULP 475 

isolating it, yet the water will remain in the mouth. As before 
stated, however, the location of a hyperemic pulp does not always 
mean the location of the cause, which may be exterior to the tooth, 
and should be looked for elsewhere before interfering with the pulp 
hyperemia. 

The prognosis of arterial hyperemia is favorable for pulp conser- 
vation in the indirect cases and in cases of cavities of decay which 
admit of cleansing without pulp exposure, or in cases of filled teeth 
if the fillings are removed, and in which the paroxysms have not 
been too severe or too often repeated. Properly protected from 
thermal shocks the vessels may recover their tone. It is also favor- 
able in cases of light blows or malocclusion, if rest of the apical tissues 
be secured. 

It would be favorable in cases of deep erosions which can be filled 
with non-conductors; but this condition is rarely seen in erosion. 
It is favorable in fractures without exposure if caps can be secured 
in place, but is unfavorable in ordinary abrasions unless so much 
deeper than the general occlusal level, that filling can be placed, or 
in sound teeth the pulps of which are irritated without evident cause, 
and in cases in which filling removal would not leave room for non- 
conductors. In cases of actual exposure of the pulp it contra-indicates 
attempts at conservation, except in the mildest varieties and most 
favorable circumstances, and then only when conservation is 
important. 

Treatment. — The therapeutic principles involved in the treatment 
of this condition are the removal of the source of irritation and the 
securing of physical rest. The treatment is directed toward immediate 
relief of the existing condition and the prevention of its recurrence. 
If a carious cavity exist, it is to be freed from debris, and the grosser 
portions of the carious dentin are removed; the pulp, if unexposed, 
is to have the layer of softened dentin covering it left unremoved, if 
leathery and not disintegrated. 

Sedative agents are imperatively called for; of those used the most 
effective being the oil of cloves, or eugenol, equal parts of oil of cloves, 
and phenol, equal parts of phenol and camphor (phenol camphor), 
equal parts of phenol and thymol (thymophen), a saturated solu- 
tion of thymol in alcohol or of menthol in chloroform or menthol, 
3 parts, phenol, 1 part, or solutions of cocain. Thymol or menthol 
crystals may be added to any of these. Dentalone and Phenandyne 
<and the fluid of "Jodoformagen" are valuable proprietary prepara- 
tions. These agents are all germicides as well as sedatives, and, 
therefore, sterilize the dentin of cavities in which they are sealed. 

They are to be applied upon cotton used alone or the first pledget 



476 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

may be covered with cotton and a non-irritating varnish, as inspissated 
tincture of benzoin, or chloro-percha, or a quick setting temporary 
cement is used as a covering or a previously prepared covering may be 
used (see arsenical covering) . In from twenty-four to forty-eight hours 
the tooth is placed under the rubber dam and excavated (if not a case 
of filling removal) ; its walls are varnished, and over the wall nearest 
the pulp a disk of softened gutta-percha is laid. Over this zinc phos- 
phate paste is flowed. " Jodoformagen" may be used in place of the 
gutta-percha. A stiff mixture of eugenol and Hubbuck's zinc oxid 
is a very valuable sedative cement to be placed against the floor 
of an excavated cavity. It hardens in saliva and may remain a 
time as a test and then be in part left as a permanent floor covering. 
After lining with zinc phosphate a gutta-percha filling may be 
introduced for a few weeks. In a case with some persistence zinc 
phosphate or gutta-percha may be used to complete the test for 
six months or a year. In mild cases the filling may be completed 
at once. The conductivity of zinc phosphate is too high to be used 
as the sole material over pulps which have been the seat of pro- 
nounced hyperemia; with varnish it is more useful. 

It not infrequently happens that it becomes necessary to assist the 
pulp arteries to recover their- tone by means of counterirritants 
applied to the gum over the apex of the root. This is especially true 
in cases of pulp capping. Dental tincture of iodin (iodin, 3iij; 
alcohol, 5j; dissolve by succussion; ] ) or potassium iodid, sat. sol., 
and zinc sulphate, sat. sol., p. seq., with iodin crystals to complete 
saturation 2 is to be applied in spots to the gums, or a mixture 
of equal parts of tincture of iodin and tincture of aconite may be 
painted upon the gum. A mixture made of two parts of tincture of 
aconite and one part of chloroform is recommended by Jack, 3 to be 
applied to the cleansed and dried mucous membrane by means of a 
pad of cottonoid, one-half inch w T ide by three-quarters of an inch 
long. It should be held in place by the finger for fifteen seconds. 
Tincture of aconite upon cotton, placed in the rubber cup-applicator 
of a cataphoric apparatus and held against the gum for a half minute 
while the current of a few cells is active, w T ill produce a circum- 
scribed area of irritation which may later lose its epidermis. This 
amount of irritation is valuable. A capsicum plaster may be used. 
For any case of obdurate pain systemic sedation or derivation may 
be employed. (See pp. 124 and 491.) 

If the pulp be exposed, it is probably the part of wisdom to remove 
it, though if for any special reason capping be demanded, it may be 

1 Flagg. 2 Northrop. 

3 American Text-book of Operative Dentistry. 



HYPEREMIA OF THE PULP 477 

done. When the hyperemia is active both cocain and arsenic may 
be resisted. 

In cases of abrasion or erosion an obtundent is applied; an exca- 
vation having a retentive form is made, which is varnished in the 
pulp direction only and filled with preferably a combination of 
cement and metal; or in abrasion the pulp may require removal. 
A tooth containing a large metallic filling must have the filling 
removed, and after reducing the hyperemia a non-conducting 
layer must be placed between the pulp and the filling. The precau- 
tion should always be taken, when the pulps of teeth in which 
cavities have been prepared respond unduly to the temperature 
test, to cover the dentinal walls with a layer of non-conducting 
material. In the absence of this precaution the constant overstim- 
ulation of the pulp by thermal impulses conducted through the 
metallic filling may at any time result in hyperemia. The same 
precaution is necessary in any very deep cavity. It is also well 
to avoid fibril irritation by acid of cement, septic cement, or thermal 
shock when crowns are to be used on vital ground teeth. This may 
be done by using a thin varnish of gum damar in chloroform plus 
hydronaphthol over the tooth, and by adding powdered thymol to the 
cement and in some cases by lining the crowns and posts with chloro- 
percha (see end of chapter on .moist gangrene). If mild hyperemia 
occur after filling with metal, it ordinarily passes away after a few 
weeks. The fibrillar at first rebel, then become tolerant, owing to 
tubular calcification, etc., see page 449. 

In the cases due to hypersensitive dentin the powerful coagulants 
silver -nitrate, formaldehyde, etc., are to be tried. (See Hyper- 
sensitive Dentin.) 

In cases due to apical irritation not only must counterirritants 
be applied to the gum, but it may be necessary to cap an adjacent 
tooth with a rubber dam guard in order to guard against the irri- 
tation of the apical tissue by overocclusion. (See Acute Apical 
Abscess, Fig. 549). 

If the hyperemia is of a gradual onset and due to an overoccluding 
filling or crown, this, is, of course, to be reduced to normal occlusion. 
If due to the overocclusion induced by chronic pyorrhea, the over- 
occluding tooth is to be shortened. If of acute onset, a guard may 
also be necessary. As illustrating its effectiveness in combination 
with removal of the cause, may be cited a case of an upper third molar 
•with a small pyorrhea pocket on the mesiolingual aspect of the root. 
It overoccluded one thirty-second of an inch, each bite producing 
excruciating local pain, with also reflex to the ear. In twenty-four 
hours' use of the guard, the pocket having been treated, the occlusion 



478 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

was almost normal, the reflex pain gone, and the guard was removed 
and the tooth brought to normal occlusion. In all cases of cause 
external to the tooth the cause alone is to be treated. Trichloracetic 
acid, or silver nitrate in saturated aqueous solution, may be applied 
to inflamed bone or aphthae; while "dry socket" or exposed and 
ulcerated alveolus surface must be treated as indicated. (See Index.) 
The patient is to be directed to avoid the use of very cold or hot 
substances. 

In idiopathic hyperemia the pulp usually requires devitalization, 
though counterirritants may be tried. 

The test of success of remedial measures is the gradual reduction 
of response to slight variations in temperature — i. e., the pulp grad- 
ually bears higher and lower temperatures until, approximately, 
a normal tolerance is established. 

As shown by Jack, this varies for hot applications from 152° F. to 
118° F., and for cold ones from 74° F. to 32° F. 

In order to determine the rate of tolerance normal to the individual 
he suggests that sound lower incisors be isolated by the rubber dam 
and tested by throwing upon them first water at a temperature of 
80° F. The temperature of the water is then gradually lowered or 
raised until slight pain is produced by the test. The point registered 
by the thermometer will be the normal limit of thermal tolerance for 
the particular test. 

The data gained are useful in determining the progress of a case 
of hyperemia. 

A lack of success in the reduction of the arterial hyperemia is 
evidence that the more severe condition of venous hyperemia has 
supervened, or perhaps an infection has caused a true inflammation. 

When, after fair trial of conservative treatment, the pulp is per- 
sistently irritable, it should be removed. 

In the devitalization of hyperemic pulps there is often painful 
reaction to any of the means employed. Some of these pulps resist 
cocain pressure in any form even after sedation; some yield after 
sedation. Sedation or depletion should precede arsenical applica- 
tions, and if at any time arsenic produce a painful hyperemia or 
aggravate one previously existing, it must be removed and sedatives 
used before its renewal, or it may be applied at another portion of 
the tooth while sedatives are kept against the pulp. 

It is evident that such a grade of vascular excitement as exists in 
cases of exposed dentin is quite capable of producing the constructive 
diseases of the pulp described as secondary dentin and pulp nodules. 
On the other hand, inflammation of the pulp has produced resorption 
of the walls of the pulp chamber. 



HYPEREMIA OF THE PULP 479 

Pulp Irritation from Electric Action. — It is of quite common occur- 
rence that galvanic electricity causes pulp irritation. The cataphoric 
current too long continued may induce a hyperirritability of the 
pulp amounting in some cases to evidence of hyperemia, which 
may subside under proper treatment or eventuate in pulp death from 
venous hyperemia. The occasional connection of a newly placed or 
bright amalgam filling with a gold filling, bridge, plate, or clasp, 
through the medium of saliva or food (which amounts practically 
to the same thing), will, at times, produce painful galvanic shocks in 
a vital tooth. Dr. Franz Trauner 1 has reported that such pain has 
been felt in devitalized teeth. This is outside of the editor's experi- 
ence, and should not occur in totally devitalized teeth, as the electric 
current is a test for pulp vitality. The mouth mirror, or a fork or 
pin, touched to a new amalgam filling, may also produce the pain, 
but a nickelled steel instrument usually does not. 

Painful shock is sometimes produced by the animal electricity 
discharged from the operator during dry, cold weather. It usually 
occurs when the finger is placed upon a metal filling, or the plugger 
point is returned to a metal filling. Touching the metal part of the 
chair before approaching the patient will obviate this disagreeable 
contact. 

Treatment. — With cataphoresis, the mischief being accomplished, 
the case must be treated as other arterial hyperemias. 

In the case of shocks from the presence of the two metals it may 
be ignored if slight and the filling new, as it will probably soon pass 
away. A well-set and brightly polished amalgam filling may be 
tarnished if necessary by touching it with a 1 per cent, solution of 
silver nitrate; or, if good color be a necessity, the pulp of the tooth 
may be well insulated by means of a gutta-percha substratum, or 
the pulp may be devitalized. If the fillings be in adjoining teeth, 
they should be contoured so as to touch persistently if possible. If 
in the same tooth, the fillings should be connected by either amalgam 
or gold. 

Venous Hyperemia of the Pulp. — Definition. — By venous or passive 
hyperemia of the pulp is meant a condition of the pulp in which 
the return of the blood in the pulp to the heart is mechanically 
prevented. 

Causes, Pathology, and Morbid Anatomy. — But two causes seem 
competent to produce such a venous hyperemia. These are: (1) A 
preexistent arterial hyperemia; (2) thrombosis of vessels at the 
apex of the pulp canal. The venous hyperemia which is the second 

1 See Dental Cosmos, 1903. 



480 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

stage of inflammation is to be remembered, but excluded from present 
consideration. 

In arterial hyperemia the excess of blood is contained in enlarged 
capillaries and arterial trunks. The enlarged main trunks or trunk 
at the apex of the pulp must compress the veins, as the apex of the 
canal is unyielding. In proportion to the severity of the arterial 
hyperemia, therefore, are the emergent veins unable to remove the 
blood collected in the capillaries and venules, which gradually enlarge 
into varicosities in consequence. 

It has been shown by Hopewell-Smith 1 that thrombosis of the 
small veins and capillaries throughout the pulp may result in rupture 
of the arteries, and hemorrhagic extravasations occur — either single 
or multiple. These he terms hemorrhagic infarcts, although the 
description given more accurately denotes a minute venous hyper- 
emia. (See Fibroid Degeneration of the Pulp.) 

Black has shown that the diapedesis of red corpuscles, which is a 
characteristic result of engorgement of the veins in venous hyper- 
emia, occurs in the pulp. Edema, which usually accompanies venous 
hyperemia in other situations, cannot well occur in the pulp because 
of its unyielding surroundings (Fig. 418). 

It is possible, however, that fluid may exude into the perivascular 
spaces, compressing the cellular elements. Black has shown that 
deposits of lymph may thus occur in pulpitis. The intense conges- 
tion and distention of the vessel walls permit a free diapedesis of 
red corpuscles into the pulp tissue. Disintegration of the red cor- 
puscles may occur and the hemoglobin matter of the corpuscles may 
be diffused through the dentin, giving it a pink discoloration tech- 
nically known as "suffusion." The infiltrated dentin may then 
become progressively discolored through the characteristic changes 
of color noted in connection with graducmy decomposing hemoglobin 
— becoming purplish, dark blue, and finally blue black. The color 
may pass into the yellow or brown coloration (see Tomes' case). 
Cases have occurred of coronal suffusion in which the pulp vitality 
has persisted for months. In some cases the bulbar portion alone may 
be dead. Partial gangrene and the general darkening of the tooth 
may be present even in a single-rooted tooth with the pulp partly 
alive. This is proof that collateral circulation exists in the pulp. 
In cases of suffusion even all the root of a molar may be suffused, 
and pericementitis, associated with such a hyperemia, seems partic- 
ularly intractable. The vasomotor paralysis is extreme. 

Tomes 2 records a case of a blow upon four upper incisors, which 

1 Dental Cosmos, 1907. 2 Manual of Dental Anatomy. 



HYPEREMIA OF THE PULP 



481 



became loose and painful. A few days afterward reddish spots 
appeared upon the labial surface, which later became dark blue. 
These disappeared except for a slightly yellowish tint. Four years 
later the pulps were found vital and healthy. This rare case is con- 
firmative of the previous statements. 

If a tooth receive a blow of sufficient severity, its pulp may die 
without much evidence of pulp pain. On the other hand, if the 
blow be less severe, it may give evidence of an arterial hyperemia, 
gradually increasing in severity. 

Fiar418 






ffl 



:' ilHliJ 



!i. 




■A/ ■ *ffcm 

b (/ 

Section of hyperemic pulp, showing aneurysmal dilatation of the vessels, extra- 
vasations of blood, and red blood disks escaped apparently by diapedesis: a, a, dilated 
vessels; b, b, b, extravasated blood. Besides this, red blood disks are plentifully 
distributed everywhere in the neighborhood of the veins. The tooth was extracted 
during a paroxysm of pain. (Black.) 



In the former case it is probable that the bruising of the apical 
tissue produces a condition of thrombosis at the apex which involves 
the pulp by shutting off both its afferent and efferent vessels. A 
stagnation results, and death from lack of nutrition occurs. This is 
also termed "jugulation." 

In the latter case the thrombosis has not occurred, but an arterial 
31 . 



482 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

hyperemia is set up by the overflow of blood from the apical tissue 
into the pulp, and goes on to venous hyperemia. 

It is quite probable that rapid death of the pulp in pulpitis is due 
to the associated venous hyperemia. 

Kirk 1 mentioned an interesting case of venous hyperemia with 
intense suffusion of all the teeth as the result of hanging. In such a 
case there was arterial blood supplied to the teeth, but the venous 
flow was checked. 

Symptoms. — The symptoms of this condition, in the absence of 
definite data, can only be inferential. When the paroxysms of pain 
are continuous, instead of temporary — that is, when the pain, instead 
of temporarily subsiding, maintains a constant intensity for hours 
and does not respond promptly to sedative therapeusis, and is accom- 
panied by a sense of fulness rather than sharp agony — a condition 
of serious venous congestion is inferred. The case from which Fig. 
418 was taken had been the seat of intense paroxysmal pain for some 
hours. Upon close approach to such a pulp, blueness of the horn 
instead of pinkness may sometimes be seen. 

Prognosis. — Perfect recovery from this condition is extremely 
doubtful, so that if the pulp be not intentionally devitalized and 
removed, it will undergo degenerative changes. The fact that pulps 
have remained alive for years, after having been the seat of marked 
congestion, scarcely warrants the attempt to save so seriously 
crippled an organ. 

Treatment. — The prognosis being doubtful, the pulp should be 
obtunded and devitalized. If the pulp pain does not yield to seda- 
tives, it should be gently exposed if the excavation does not accom- 
plish its exposure. An antiseptic is to be applied, and by means 
of a very sharp puncture probe the pulp is to be delicately punctured. 
A free flow of blood follows, which relieves the vascular engorgement. 
When this is accomplished the cavity is to be syringed out with 
warm water, and a pellet of cotton containing a saturated solution 
of menthol in chloroform may be sealed in the cavity, or simply 
retained by means of a second pellet of cotton saturated with in- 
spissated tincture of benzoin or chloro-percha. After twenty-four 
hours an arsenical application may be made for the purpose of 
pulp devitalization, or the pulp may be removed by other means if 
tolerated. If desired, the bulb of the pulp may be taken out under 
general anesthesia, or the whole pulp under mucous, or conductive 
anesthesia (see p. 407), or, possibly, under cocain pressure anesthesia, 
though intense hyperemia counteracts, as a rule. 

1 Private communication. 



INFLAMMATION OF THE PULP 483 

The extreme paralysis of the vessel walls is occasionally shown by 
persistent hemorrhage after depletion, and which resists ordinary 
effort at limitation. In some cases the intense pain may continue 
as well. The application to the pulp of a mixture of powdered 
thymol and dried alum, equal parts, taken up on a pellet of cotton 
moistened with a saturated solution of thymol in alcohol, has proved 
useful in some cases. A general anodyne may be required for relief 
of the pain. 

INFLAMMATION OF THE PULP (PULPITIS). 

Definition. — Pulpitis is the occurrence of the phenomena of inflam- 
mation within the pulp tissue. The characteristic emigration of 
leukocytes from the bloodvessel into the perivascular tissues must 
have occurred. 

Causes. — This morbid anatomy is usually found associated with 
diseases of the tooth crown or pericemental tissue which admit 
bacteria to the pulp. At the same time it is quite probable that 
a non-septic irritant, such, for example, as a partially absorbed 
extravasation of red corpuscles or undue pressure of a filling upon a 
thin lamina of healthy dentin overlying the pulp, or as has occurred 
of a metal filling upon or even extending into a pulp, or an escharotic 
applied to the pulp may induce the characteristic pathology of 
inflammation which may be non-septic or septic according to the 
sterility at the time of operation. 

According to the character of the cause, therefore, inflammation 
of the pulp may be divided into simple and infective. It may be 
that a simple inflammation may become an infective one owing 
to the association of bacteria — e. g., the pressure of a foreign body 
may initiate the process and the inflamed pulp become a soil for the 
propagation of the bacteria present. 

The causes of pulpitis may be grouped under three headings : 

1. Mechanical or physical causes, which irritate by acting as 
foreign bodies, or by pressure. 

2. Chemical causes, which act as irritants by either producing a 
chemical destruction of pulp tissue, or by irritation without direct 
destruction. In the former case the dead tissue acts as a foreign 
body against which the pulp reacts in an effort to cause its exfoliation 
or absorption. 

« 3. Parasitic or infective, which cause the phenomena of infective 
inflammation. 

Pulpitis is classified, according to its extent, into partial and com- 
plete; according to its duration, into acute and chronic; according 



484 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

to its infective character, into purulent and non-purulent; and, 
again, according to the character of the degeneration which follows 
upon the inflammatory process. While pathologically these con- 
ditions may be clearly differentiated from one another, they may be 
reduced to more compact groupings according to their clinical sig- 
nificance. For example, acute pulpitis is frequently infective, partial, 
and purulent; chronic pulpitis is frequently non-infective, extensive, 
non-purulent, and followed by secondary degenerations. It is, 
however, often purulent, and, of course, infective. 

For the sake of convenience, pulpitis will receive a clinical division 
into acute and chronic. 

Acute Pulpitis. — By acute pulpitis is meant that form of inflam- 
mation of the pulp which runs an active and more or less violent 
course toward pulp death, and has associated with it acute par- 
oxysms of pain. 

Causes. — The causes of acute pulpitis are direct and indirect, 
intrinsic and extrinsic; the vast majority of cases being due to 
extrinsic causes. The direct intrinsic causes are hemorrhagic extra- 
vasations accompanying venous congestion, or thrombosis (In- 
farction), pulp nodules, and injury of the vessels at the apex of the 
root. The direct extrinsic causes are, perhaps, invariably associated 
with, bacterial invasion, a possible exception being the pressure 
of filling material upon a thin elastic lamina of softened dentin, 
covering the pulp. The dental pulp is intolerant of the slightest 
pressure, and rebels vigorously when subjected to compression. 
Irritating drugs may also act as irritants — e. g., zinc chlorid. It is 
not necessary that the pulp should be exposed to permit bacterial 
infection, and extensive bacterial invasion is probably not necessary 
for the production of pulpitis. The waste products, ptomains, etc., 
of bacteria may find their way to the surface of the pulp via the 
dentinal tubuli, through a layer of softened dentin, and excite 
inflammation. It is extremely probable that infection of the pulp 
is an invariable consequence of its exposure by decay; but as a 
pulp may be exposed without subjective evidences of hyperemia or 
inflammation, it follows that infection does not necessarily imply 
inflammation, though the absence of acute symptoms may be 
accounted for by the escape of the effusions into the cavity of decay. 
The presence of a gross irritant, such as a mass of food debris, 
vegetable seeds, bread crumbs, etc., in contact with the pulp will 
precipitate an acute inflammation in which bacterial relations must 
be taken into consideration. 

"The severity of the inflammation does not appear to be pro- 
portionate to the number of bacteria present, and in a highly in- 



INFLAMMATION OF THE PULP 



485 



flamed pulp we may be able to find but few bacteria. . . . The 
conclusion seems to be justified that the inflammation is due to 
the combined action of the bacteria and their products (acids, 
ptomains, etc.) with which the carious dentin becomes impregnated." 1 
Goadby has shown that the Streptococcus brevis and Bacillus 
necrodentalis may pass through the tubules of even secondary 
dentin. 

Pulpitis from injury of the vessels at the apex of the pulp must 
be mentioned. It may occur in consequence of blows, biting upon 
hard substances, too rapid wedging, the rapid movement of teeth 
in orthodontia, 2 and the progressive loosening of teeth in pyorrhea 
alveolaris. In these cases the pericementum is primarily affected 

Fig. 419 




Inflammation of dental pulp: a, a, normal cells; b, b, b, b, inflammatory elements; 
c, cells in process of division (y 7 inch.) (Black.) 



by a non-septic pericementitis which extends into the pulp, producing 
arterial hyperemia as an accompaniment, and the teeth are tender 
upon percussion as well as sensitive to thermal changes. In these 
cases the pulp may have either hyperemia or non-septic pulpitis, 
impossible of differentiation unless the tooth be extracted. Pain 
in the teeth upon assuming the recumbent position, dull, heavy 
uneasiness about the jaws, and inordinate response to thermal 
stimuli, particularly to heat, point to pulpitis. Bacteria from an 
abscess on an adjoining tooth or from a pyorrhea pocket when 
these actually reach the apical region of the tooth in question may 

**■ Miller: Dental Cosmos, 1894. 

2 Buckley, through a circular letter to orthodontists, obtained opinions that the 
upper centrals and laterals are most liable owing to the frequency of displacement, 
character of movement, prominence of location, and the curve of lateral roots. Items 
of Interest, December, 1910. 



486 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 



infect a pulp from the apex. This will cause the death of a single 
pulp, but only inflammation in a multirooted pulp. Infection by 
way of the blood stream is a possibility. The pressure of an impacted 
tooth may also act as a cause by pressing the apical tissue, or by 
causing resorption of the root (see p. 292). 

Morbid Anatomy and Pathology. — In determining the existence of 
pulpitis, no matter what the symptoms which have presented or the 
condition as to exposure, etc., the microscopic examination of sections 
of the affected organ constitutes the only decisive test; if the changes 
characteristic of inflammation be absent, no matter what the symp- 
toms, pulpitis did not exist. The essential feature of the process is 

Fig. 420 




Interstitial pulpitis with pulp nodule in situ. (V. A. Latham.) 



emigration of the white blood corpuscles from the small veins into the 
intercellular matrix of the pulp. At first the inflammatory elements 
(leukocytes) are scattered through the spaces between the pulp cells 
(Fig. 419) ; at a later stage the territory is occupied by round indif- 
ferent cells alone. The inflammation may be widespread, as shown 
in Fig. 420, or may be localized to some portion of the pulp, as one 
horn of a pulp; Black noted also inflammatory action occurring in 
small islands (Fig. 421). 

Swelling of the pulp (from exudation) cannot occur unless there be 
a break in the wall of the pulp chamber through which additional 
space can be gained. Black has recorded that "he found beneath the 



INFLAMMATION OF THE PULP 



487 



layer of odontoblasts in the region of an exposure an unmistakable 
deposit of inflammatory lymph. The case had a history of severe 
toothache for two days, two weeks previously. The pulp exhibited 
evidences of previous extravasations of blood from hyperemia." 

There is evidence that the pulp may recover from attacks of 
inflammation, and that resolution occurs. In some cases, as shown 
under the head of calcareous degeneration, the tissues may become 
infiltrated with calcic material. In others, chronic degenerative 
changes — inflammatory degeneration — may supervene. 




Minute inflammatory focus -within the tissues of the pulp: a, a, arterial twigs; 
b, a nerve bundle; c, collection of leukocytes. (Black.) 

Suppuration of the pulp is a common accompaniment of pulp 
inflammation; this, being necessarily infective, will be described 
separately. 

Gaskell 1 has reported a case where a central incisor entirely free 
from caries exhibited on its palatal aspect a pinkish tinge, w T hich 
increased in depth until the enamel overlying crushed in, revealing 
the pulp of the tooth lying immediately beneath; there had been a 
resorption of a large mass of the dentin lying between the pulp and 
the enamel. The pulp was removed and the tooth filled. No history 
is given as to the condition of the root, whether resorption had 
occurred there or not. Shortly after, the adjoining central incisor 
exhibited a like pink coloration, which increased, leading to the 
inference that resorption was in progress in this tooth also. At the 
suggestion of E. C. Kirk the patient received continued doses of 



Proceedings of the Academy of Stomatology, Philadelphia, 1895. 



488 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 



arsenic iodid and the compound syrup of the hypophosphites, in the 
hope of inducing a general and local constructive metamorphosis. 
This treatment was followed by a gradual disappearance of the pink 
coloration, an evidence of a redepositionof dentin. In the absence 
of histological data it is impossible to state just what was the nature 
of the repair tissue in this particular case, but Miller 1 has shown 
that the pulp may take up a resorptive function and remove dentin 
which may later be redeposited as anomalous tissue. The new 
dentin does not contain tubules, but has the characteristics of 
cemental tissue 2 (osteodentin), or even bone with Haversian systems 3 
(Fig. 422). This process has its analogue in the tusks of elephants 
and also in the production of Howship's lacunae in the resorption of 
the pericementum, these lacunae later being filled up with cementum. 

Fig. 422 




Resorption of the walls of the pulp chamber and redeposition of new calcific matter: 
a, pulp chamber; b, c, d, portions of resorption areas not refilled and walled off by the 
new deposit-forming cavities occupied originally by the pulp tissue. (Miller.) 



There have been cases of inflamed pulp in teeth decayed while 
yet impacted. In these cases there is usually some form of sinus 
connecting the tooth with the mouth. 

Symptoms. — The early stage of inflammation is an arterial hyper- 
emia, and as the leukocytes collect in the venules a venous hyperemia 
is established. No matter how far the area of stasis extends, beyond 
it will exist an area of arterial hyperemia. Owing to the enclosing 



1 Dental Cosmos, August, 1901. 

2 Hopewell-Smith: Histology and Pathohistology of the Teeth. 



Salter. 



INFLAMMATION OF THE PULP 489 

canal walls and constricted apex a general venous hyperemia may be 
established which causes the death of the pulp. 

In view of these facts it is not surprising that the symptoms of 
pulp inflammation take on somewhat the characteristics of both 
arterial and venous hyperemia. The diapedesis of leukocytes and 
exudation of fluid cause the phenomena of heavy, boring pain and 
a feeling of internal pressure. 

The pulp may be exposed and no symptoms be present. A sudden 
pressure of food or toothpick, suction upon the pulp or the contact 
of cold or hot, salt, sweet, or acid substances, may excite an attack 
of throbbing or lancinating pain. This may be localized in the tooth 
or may be reflected to other teeth or the parts mentioned under 
hyperemia (p. 471). 

The assumption of the recumbent position permits an increased 
flow of blood into the paretic vessels of the pulp and increased suffer- 
ing results in correspondence with the law that inflamed parts are 
always more painful in the dependent position. (See p. 131 and 
201.) Indeed, recumbency is sufficient at times to induce a 
paroxysm in a comparatively quiet but inflamed pulp. Under a 
capping or filling pressing on the pulp or thin dentin the pain may 
begin as a slight pain and gradually increase in intensity, or it may 
respond as a sudden agony, beginning even some time after the 
operation. This may have been known at the time of operation or 
been suspected later. In one typical case, violent reflexes occurred 
sometime after a metal filling was introduced over sound dentin. 
The diagnosis was uncertain but filling removal and placement of 
eugenol and zinc oxide cement for a month, removed the reflexes, 
permanent filling was done and after a year no trouble exists— diag- 
nosis, pressure irritation. In the later stage of pulp inflammation 
the pain is of a heavy, boring, continuous character, the perice- 
mentum becomes somewhat hyperemic, and the tooth responds to 
tapping. In case of a highly irritable pulp, however, the concussion 
of the pulp produced by tapping may readily cause pain. 

In pulpitis the pulp responds both to heat and cold, but, as a rule, 
more to the former than to the latter. There have been many cases 
of reflex neuroses developed by inflamed pulps, reflex pains in the face, 
eye, ear, neck, scalp, chest, arm, heart, etc., as well as functional 
disorders of the eye, ear, and brain. One case of dementia prsecox 
was cured by removal of a tooth with inflamed exposed pulp. 1 One 
case of sensory paralysis of the entire left side w r as caused by inflam- 
mation of a portion of the pulp in a right upper cuspid and marked 

1 Upson: Dental Cosmos, 1910, p. 529. 



490 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

relief began in about an hour after removal of a covering dressing 
and filling. The symptoms of suppurative inflammation may differ 
somewhat (see Abscess and Ulceration, p. 492). 

Diagnosis. — The diagnosis is largely inferential and made by 
observation of the symptoms and conditions existing. The pulp 
may be exposed or closely approached by caries, or the pulp may 
be approximated by a large filling. If there be a leak about the 
filling, a septic fluid or actual decay beneath the filling may be the 
exciting cause. In the absence of evident causes such sepsis is always 
to have consideration, and, if necessary, the filling must be removed 
and tests applied. The more obscure causes, such as abscesses upon 
adjoining teeth, infection from the pericemental tract in the course 
of pyorrhea, looseness of teeth or traumatisms, are to be carefully 
considered. If the tooth involved be uncertain, each tooth should 
be placed under rubber dam and tested thoroughly. 

Prognosis. — The prognosis is always bad for the comfortable 
conservation of the pulp, and it should be removed and the canal 
filled. 

Treatment. — The treatment of pulpitis involves the reduction of 
the amount of blood in the vessels of the pulp, the sterilization 
of the infected area, the relief from the pain, and the removal of 
the pulp. It is usual to excavate the cavity of decay thoroughly 
enough to remove from over the pulp decayed dentin which would 
prevent the action of remedies or act as an irritant. The cavity is 
then washed and a sedative applied. (See p. 475.) A creamy paste 
of bicarbonate of soda in carbolic acid has been recommended. 1 
The addition of a trifle of powdered alum to any of the sedatives 
acts as an astringent to the vessels. During the half hour succeeding 
the application the pulp should give some indication of relief. If 
it be somewhat decided, a portion of the remedy used should, if 
possible, be sealed in the cavity for twenty-four hours. The covering 
may be prepared first as for arsenic. (See p. 527.) If not possible 
to seal it in, it may be covered with cotton saturated with a varnish 
made by evaporating tincture of benzoin. This varnish hardens 
like sandarac varnish, but, unlike it, is not irritant. Claims are 
made for alcohol used as for pressure anesthesia. 

If after the first half hour no indication of relief has been obtained, 
it is well to expose the pulp and to relieve the engorged vessels by 
delicately puncturing it. (See Extirpation of Pulp.) After exposing 
the pulp it will perhaps exude a bead of pus, which makes the diag- 
nosis one of pulp suppuration. After free bleeding, which may be 

1 Gerdtzen. 



INFLAMMATION OF THE PULP 491 

encouraged by means of warm water, the sedatives will usually act. 
It may be necessary at times to employ short general anesthesia 
(nitrous oxid gas, etc.) as a means to obtain free bloodletting. Every- 
thing being prepared, the patient is anesthetized and the bulb of the 
pulp cut out, or if N 2 and O anesthesia can be used, the entire pulp 
may be taken out. At times cocain pressure anesthesia is effective 
at least for the removal of the bulb of the inflamed pulp, and some- 
times of the entire pulp; often, however, it causes too much pain. 
When several trials have been made, and even the cotton forced 
into the pulp tissue without complete anesthesia, a pellet of devi- 
talizing fibre may be put into the pulp chamber with no discomfort. 

In case of partial extirpation, not only is free bleeding induced, 
but the diseased pulp tissue is largely removed. When hemorrhage 
ceases arsenic may be applied, or pressure anesthesia attempted. 
If the hemorrhage be obstinate the application of powdered thymol 
and dried alum may be used. (See Venous Hyperemia.) W r hen 
sedatives are used upon the pulp, counterirritants applied to the 
gum are aids of great value, and are to be used as described under 
Arterial Hyperemia (p. 476). 

In addition to these the principle of depletion may be employed. 
Deep cuts may be made with a sharp bistoury in the gum overlying 
the root apex. The anastomosis with the vessels of the apical tissue 
is expected to cause the cuts to act as openings made in veins leading 
from the inflamed pulp. According to Nancrede, depletion on the 
venous side of an inflamed area markedly reduces engorgement. In 
addition to these measures catharsis is a valuable means of derivation; 
a tablespoonful of sulphate of magnesia is to be dissolved in a goblet 
of water and taken internally at least a half hour before a meal. 

If the pain be obdurate and its return feared, two f grain sulphate 
of morphin tablets may be dispensed, preferably by the operator, 
to be taken only in case of severe pain and an hour apart. 
Acetanilid and phenacetin are also useful. 

The following is a useful anodyne and antineuralgic prescription: 

1$ — Acetphenetidini (phenacetin) , 

Acetanilidi aa gr. xxx 

Quininse sulphatis gr. xv — M. 

Pone in capsulas no. vi. 

S. — One morning and evening. 

(See also Treatment of Facial Neuralgia.) 

Hall 1 has suggested : 

3 — Aspirin 5ss 

Codein gr. iss 

M. et. ft. chart. No. vi. 

Sig. — One every half-hour until relieved. 

1 Dental Cosmos, 1910, p. 1085. 



492 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 



Trigemin is also useful. 

Quiet of the pulp must be secured before an arsenical application 
is made, or the latter merely increases the irritation instead of 
promptly devitalizing (an exception is noted above). Should such 
an irritation occur or be feared, arsenic may be sealed in an opening 
made in another part of the tooth (a "pocket" 1 ), with a view to 
devitalizing the pulp through an avenue of healthy pulp tissue. At 
the same time the pulp may be quieted by sedative applications 
made in the cavity of decay. 

Instead of drilling a special pit, the arsenic may be applied at a 
portion of healthy dentin in the cavity, which is at some distance 
from the orifice of exposure; over the latter the analgesic may be 
placed (see p. 515, etc.). 



Fig. 423 



SUPPURATION OF THE PULP. 

Definition. — By suppuration of the dental pulp is meant a forma- 
tion of pus on its surface (ulceration) or in its substance (abscess). 
It occurs both as an acute and as a chronic affection. 

Causes. — The immediate cause of suppuration of the pulp is the 
ingress of pyogenic organisms to the pulp. As in inflammation of 

the pulp, while usually associated with 
direct exposure of the pulp, suppuration 
may occur in pulps covered by softened 
or even unsoftened dentin. 

Arkovy 2 first observed infection of 
the pulp while still covered by a layer 
of unsoftened dentin (Fig. 423). 

Goadby has shown that microorgan- 
isms may penetrate even secondary 
dentin, a condition not infrequently seen 
(Fig. 423). Miller states that sections 
of the overlying dentin in a case of sup- 
puration of the pulp showed the same 
forms of bacteria as were found in the 
pulp itself. 
Bacteria which have entered the body through wounds, etc., may 
be deposited in the pulp as well as in any other part of the body, 
wherever there may be a lessened resistance at the time. While 
bacteria may thus enter from the circulation, there is usually abun- 
dant opportunity for their entrance from the mouth. Suppuration 




Invasion of pulp by micrococci 
(Arkovy.) 



1 Flagg. 

2 Diagnostik der Zahnkrankheiten. 



SUPPURATION OF THE PULP 



493 



of the pulp is a not infrequent sequel of the capping of pulps which 
have given evidence of a previous hyperemia or inflammation. 

Morbid Anatomy and Pathology. — Anatomically pulp suppuration 
(purulent or pyogenic pulpitis) is of two general varieties : one begins 
upon or close to the suface of an exposed pulp, and gradually destroys 
the organ through a process of progressive ulceration (Fig. 424); 
the second, that confined in the substance of the pulp, causes the 
gradual destruction of a part of the pulp through the formation of 
circumscribed abscesses (Fig. 425). 

Fig. 424 




A, diagram of lower molar with caries at a which exposes the pulp; the darkened 
portion at b shows the extent of the inflammation; the rest of the organ was free from 
inflammatory change. B, illustration of the inflamed tissue, showing a part destroyed 
by suppuration at a; the odontoblasts are undermined at b; the bloodvessels which 
were filled with blood clot in the section are left blank here, that they may be more 
apparent. (Black.) 



Ulceration of the Pulp. — Of these two forms, ulceration is the 
more common. The capillaries (Fig. 424) are blocked w T ith coagu- 
lated blood (they are left open in the illustration to clearly mark 
their position); the intercapillary meshwork is occupied by inflam- 
matory exudation; the surface of the pulp is eroded and covered with 
pus corpuscles; the ulcerative process is undermining the layer of 
odontoblasts. The suppurative process penetrates the body of the 
pulp, following the direction of its veins and hollowing out the organ 



494 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 



into a deep cavern. Black regards the persistence of the layer of 
odontoblasts as indicating an inferior vitality, as it shows they are 
less susceptible of change of form than the other cells of the organ. 



Fig. 425 




Acute suppurative pulpitis in the coronal portion; /, intensely inflamed horn; A, 
abscess; V, bloodvessels engorged with blood; S, superficially inflamed horn; N, nest 
of inflammation. X 10. (Bodecker.) 



The process of ulceration may continue for weeks or months until 
the entire organ has been destroyed molecularly. The necrotic por- 
tions undergo putrefactive decomposition, probably passing through 



SUPPURATION OF THE PULP 



495 



the same stages that any albuminous substance passes in its serial 
decomposition, into the end-products — ammonia, carbon dioxid, 
hydrogen sulphid, and water. 

"Very interesting and instructive results were obtained by exam- 
ining the material from different parts of the same tooth. In the case 
illustrated in Fig. 426 the pulp chamber at a was wide open and 
filled with food particles, which had a foul, half-putrid odor; at b the 
pulp was putrid and foul-smelling; at c there was a small abscess, 
filled with pure white pus, while the tissue between this point and 
the apex of the root was highly inflamed and bright red. Material 
from the pulp chamber (Fig. 426, a) contained the forms shown in 



Fig. 426 



Fig. 427 



Fig. 428 




Fig. 429 



v :•/ 





v '.. 






j 






--> 



Microorganisms found in cultures from gangrenous pulp. (Miller.) 

Fig. 427; material from point b those shown in Fig. 428, and from 
the point c those shown in Fig. 429. We perceive a gradual dimin- 
ution of the large cocci, and the appearance of small, delicate cocci 
and diplococci." (Miller. 1 ) The editor has observed cases of vital 
but finally ulcerated pulps under canal fillings. In one case twelve 
years had elapsed between the partial canal filling and the more 
recent observation. 

Symptoms. — If the cavity of decay be open the pus and serous 
exudate may freely escape, so that the symptoms may not exceed a 
dull, gnawing pain, which is usually reflex in character. 



* Dental Cosmos, 1894. 



496 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

As a rule, the response to cold will be much delayed or even absent. 
Intense pain may exist when the pus cannot find exit owing to food 
debris being massed in the pulp chamber, or owing to the presence 
of a filling or mass of secondary dentin. The case then resembles 
and practically becomes one of abscess of the pulp. 

The chief diagnostic feature of pulp ulceration is the presence 
of the subacute inflammatory symptoms described above and the 
presence of a pulp partially removed by decomposition of its upper 
portion. 

Thus if the pulp chamber be open at one horn, and a probe may 
be passed into it for a short distance until it comes into contact with 
an irritable portion of pulp, and when withdrawn have the odor of 
putrefaction, the diagnosis is clear — loss of pulp substance by putre- 
factive changes, presumably by suppuration. In some teeth it may 
be by partial gangrene. Many phases of this condition may be seen; 
thus in an extreme case one canal of a lower molar contained a highly 
irritable vital filament of pulp extending but one-quarter inch from 
the apical foramen; a second canal was entirely occupied by a per- 
fectly vital but ulcerating filament; the third canal contained an 
entirely dead pulp. The bulb of the pulp had disappeared, doubtless 
by suppuration. 

Treatment. — The treatment of pulp ulceration in its early stages 
involves the opening of the orifice of exposure, the sterilization of 
the superfices of the pulp, and pulp removal. 

Superficial sterilization may be accomplished by removing the 
pus or putrefactive material present by means of warm 3 per cent, 
hydrogen dioxid. The saturated solutions of thymol in alcohol or 
menthol in chloroform, or 2 per cent, formaldehyd or formocresol 
diluted to 3 per cent, formaldehyd strength may be sealed in posi- 
tion against the pulp for twenty-four hours as an antiseptic. The 
application of arsenic may then be safely made. In favorable cases 
the bulb of the pulp, or even the entire pulp, may he removed at the 
first or second sitting by means of cautiously applied cocain pressure 
anesthesia. In some cases, however, the patient will rebel. (See 
p. 515, etc.) 

When a part of the canal filaments alone remain, after syringing 
to remove pus, the pressure anesthesia may be resorted to. A long 
thread of cotton is saturated with carbolic acid or carbolic acid 
and cocain, and gently packed into the canal against the pulp fila- 
ment. Pressure with vulcanizable rubber is now produced, and after 
a few minutes the pulp will be sterilized and anesthetized sufficiently 
for removal. It is better to treat each canal separately as a general 
pressure will probably fail. Puncturing is also useful at times (see p. 



SUPPURATION OF THE PULP 497 

531). Arsenic may be cautiously placed on cotton half-way up a 
canal against such a pulp filament. Another method consists of 
packing' a thread of cotton dipped in carbolic acid tightly against 
the filament, in which thrombosis is thus induced. (See also p. 

Abscess of the Pulp. — Abscess of the pulp is usually situated near 
the point of exposure of the organ. It may be confined to one horn 
of the pulp, or may involve nearly the entire substance of the pulp, 
the peripheral tissue of the pulp being unbroken. Abscess may exist 
at some distance beneath the surface of the pulp, and the latter be 
still covered with a layer of dentin. Burchard once uncovered the 
horn of a molar pulp which was covered by a lamina of hard dentin, 
and no fluid appeared; but upon passing a sharp probe into the white 
area of exposure for over one-eighth of an inch or more there was a 
free flow of pus which quickly filled the larger carious cavity. A pulp 
removed entire from a tooth, and which was yellowish white in color 
and unbroken, showed upon section its interior hollowed out into an 
enormous abscess cavity (Fig. 431). The bloodvessels were blocked; 
the peripheral tissues were unaltered; between the odontoblasts and 
the abscess cavity, the latter lined with pus corpuscles, evidences of 
inflammation were plenty. Black found that the odontoblasts 
retained their form after neighboring cells of the pulp had been 
destroyed. 

Miller's 1 researches show a preponderance of cocci and micrococci 
in cases of enclosed abscess; cocci and diplococci w T ere of constant 
occurrence. Many of the forms, both cocci and bacilli, were cultivable 
upon gelatin and agar-agar. Some of them, cocci and bacilli, brought 
about the liquefaction of gelatin; other did not. So that it must be 
inferred that infective inflammation and necrosis of the pulp may 
occur without suppuration. (See Gangrene of the Pulp.) In some 
instances streptococci were found. In the freely exposed pulps 
varieties of organisms were found which would render clear the 
possibility of a general infection by way of the dental pulp. 

Symptoms. — The usual symptoms are as follows: In a tooth con- 
taining an enormous filling, one in which the pulp has been exposed, 
or in a tooth having a large carious cavity, the patient gives a history 
of discomfort or decided pain, appearing at intervals, sometimes 
appearing and disappearing suddenly, the existing condition having 
been ushered in by dull, gnawing pain, which is usually not positively 
located, although it may be. The pain grows in intensity, and, in 
contradistinction to the pulp conditions previously described, pain 

1 Dental Cosmos, 1894. 
32 . 



498 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 



is relieved instead of increased by applications of cold. It may be, 
however, that the prolonged contact of iced water may induce a 



Fig. 431 




Transverse section of inferior bicuspid pulp, one-half diagrammatic: a, abscess 
cavity; b, embryonic cells at the periphery of the abscess cavity; c, occluded blood- 
(Burchard.) 



Fig. 432 



response. The response to heat is marked, so that a mouthful of hot 
coffee or even the warmth of the tongue may precipitate an attack 

of severe and continued pain. 
Pain produced upon passing from 
a warm to a cold atmosphere, and 
vice versa, is also symptomatic. If 
the pulp be freely exposed and 
pricked with a sharp instrument, a 
flow of pus follows in many cases, 
and the relief is almost immediate. 
In the earlier stages a period of 
throbbing pain may follow evacu- 
ation of the pus. 

In other cases the response to 
heat may decrease until it is almost 
absent, and the case only be seen 
when evidences of the action of 
bacterial products upon the peri- 
cementum appear, which they 
usually do in the later stages of pulp suppuration, when the tooth 
becomes loose, extruded, and tender upon percussion. 




Abscess of the pulp after forma- 
tion of a large amount of secondary 
dentin, dividing the pulp into two 
portions: £ D, secondary dentin; 
V P, abscess or confined pus; I, 
area of apical inflammation. (Dia- 
grammatic.) (After case in the 
mouth.) 



SUPPURATION OF THE PULP 499 

The symptoms of pericemental disturbance may simulate those of 
incipient, acute, apical abscess, even though a quarter of an inch or 
more of apical pulp tissue exist in a vital though highly inflamed 
condition. Upon clinical evidence it is assumed that the inflammation 
of the pulp produces inflammation of the apical tissue (Fig. 432). 
In one case the gum and contiguous parts about an upper molar 
were swollen, apical abscess diagnosticated, and a free flow of pus 
followed by blood obtained upon opening the crown. An examina- 
tion made twenty-four hours later, after symptoms had subsided, 
demonstrated all three pulp filaments to be alive when a 'post hoc 
diagnosis of extensive abscess of the pulp was made. If untreated, 
symptoms of pulp and pericemental disturbance may disappear for 
weeks or months; but if the parts be not perfectly sterilized and 
reinfection prevented, it is only a question of time w^hen septic 
pericementitis will arise. 

Diagnosis. — The most valuable diagnostic symptom is the peculiar 
reaction to thermal stimuli — the decreasing, then absent response 
to cold, and the increasing reaction to applications of heat. This 
reaction, together with the continued gnawing and full sensation 
in the tooth, usually affords a diagnosis which is confirmed by evac- 
uating pus from the pulp, which exudes usually as a minute bead 
followed by blood, although the reverse order may obtain. 

In cases where several teeth are involved in the diagnosis, differ- 
entiation is made by isolation of each tooth by means of a small 
square of rubber dam. The thermal test is then applied. The pres- 
ence of a quantity of secondary dentin will confuse by causing dulness 
of response. In such case the electric test should be resorted to. 
(See Dry Gangrene.) In some cases secondary dentin will have 
formed in the pulp cavity and the abscess may be found in one of 
the filaments, while the other will be apparently healthy. Fig. 432 
is a diagram of a number of cases seen in practice. 

Prognosis.- — General experience regards ulceration and abscess of 
the pulp as precursors of the death of the organ. Usually this is 
by progressive suppuration. It is undoubtedly true, however, that 
attempts at circumvallation of the dead tissue are made in some 
cases (Fig. 433) . The pus cells undergo degeneration and the abscess 
site may be the seat of calcareous deposits. Even in these cases 
death is delayed, not averted. The remainder of the pulp under- 
goes atrophic changes, and commonly suppuration reappears. 

Treatment. — The treatment of the case consists in relieving the 
existing pain, completing the devitalization of the pulp, and removing 
it in such a manner that no organisms or dead matter are carried 
beyond the apex of the root. 



500 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 



To secure relief, evacuation of the pus is imperatively necessary. 
The organ is freely exposed, exercising no pressure in gaining free 
access to it. If pus does not flow upon exposure of the surface of 



Fig. 433 




Chronic suppurative pulpitis terminating in calcification of the pus and atrophy of 
the pulp: A 1 , larger abscess, filled with calcified pus; A 2 , abscess at the periphery of 
the pulp; A 3 , A 3 , small longitudinal abscesses, all calcified; N, calcified nerve bundle; 
C, C, calcareous depositions in the fibrous pulp tissue; P, P, pigment clusters from 
previous hemorrhage. X 10. (Bodecker.) 



the pulp, a sharp, slender, sterilized probe is quickly passed into the 
substance of the pulp, when, if pus be present, it will usually escape 
freely through the opening thus made and be followed by blood. 



CHRONIC INFLAMMATION OF THE PULP 501 

If the pus formation be limited and circumscribed, throbbing 
pain may follow, which a sedative promptly quiets. The application 
is not made until the pus flow ceases. A pellet of cotton wet with a 
1 per cent, solution of formalin, or a saturated solution of thymol 
in alcohol or other antiseptic sedative, is laid upon the pulp and 
the cavity is sealed for twenty-four hours (never longer), and then 
the pulp is removed. Should the exposed portion of the pulp be 
insensitive it is cut away until access is had to the vital portion, 
where the arsenic is to be applied. The pulp may sometimes be 
anesthetized by cocain for removal. The rubber dam need not 
necessarily be applied for the treatment preliminary to devitalization, 
but the pulp should be kept under the influence of antiseptics. (See 
p. 515, etc.) 

CHRONIC INFLAMMATION OF THE PULP. 

In cases in which the resistive force of the pulp is great and the 
causes of less violent nature or less violent in action, the inflammation 
may be of low grade and continue for some time. Pulp ulceration 
may pursue a chronic course, as has already been described. Abscess 
of the pulp may also become chronic, and the pulp may even encap- 
sule the pus area, and, the bacteria dying, the abscess area may 
become the seat of calcareous deposits. 

Fig. 434 




Chronic inflammation of the pulp, areolation, and degeneration (Black.) 

Sclerosis of the Pulp. — Inflammation of a low grade may persist 
in the pulp for long periods, giving rise to an increase of its fibrous 
tissue with atrophy of the cellular elements, producing a condition 
found in chronic interstitial inflammation in some other tissues — a 
sclerosis. Instead of the usual distribution of myxomatous tissue, 
bands and bundles of fibrous tissue appear. The pulp appears 
shrunken and stiff, bloodvessels are contracted and sclerotic, and 
the nerve fibres have undergone partial or complete atrophy and 
degeneration (Figs. 434 and 435). 



Fig. 435 




Pulpitis arteriosclerosis; nerve degeneration. (V. A. Latham,) 



Fig. 436 




A, a first lower molar with a cavity at a completely filled by an hypertrophy of the 
pulp, which has grown out through the orifice, exposing the pulp at b. B, a field 
illustrating the tissue of the growth, which is composed almost entirely of granulation 
tissue of a very primitive type; a, a covering of epithelium presenting papillae; 6, 
epithelium apparently without papillae. (Black.) 



CHRONIC INFLAMMATION OF THE PULP 503 

Black found that in the late stages of sclerotic atrophy areolae 
developed in the bundles of connective tissue, the inflammatory 
elements having disappeared and the areola? being occupied by 
fluid. Arkovy describes the condition as reticular atrophy of the 
pulp (Fig. 434). 

Sclerotic and other chronic degenerations of the pulp usually 
present the history of one or more attacks of pulpitis in the past, 
with more or less continuous uneasiness extending over a long period. 
The response of the pulp to all tests becomes diminished and dull. 

Treatment. — Such pulps are to be devitalized and removed. 

Chronic Hyperplastic (Hypertrophic) Pulpitis. — When the pulp 
is exposed over a wide area, long-continued chronic inflammation 
may lead to an enlargement of the organ with a protrusion of an 
altered pulp mass through the orifice of exposure, producing the 
condition known clinically as fungous pulp. When the growth 
extends beyond the boundaries of the orifice and then increases in 
bulk it forms a pedunculated mass to which the term polypus of the 
pulp has been applied. 

Morbid Anatomy and Pathology. — The growth has its origin in a 
chronic inflammation of the body of the pulp; the organ swells, and 
contact with the sharp edges of the orifice of exposure excites a 
continued irritation, leading to further proliferation of the cells of 
the inflamed part, so that a large mass of embryonic tissue is formed 
(Fig. 436), termed by Black granulation tissue of a low type. As in 
the granulation tissue of repair, bloodvessels grow into this mass, 
so that it may bleed at a slight touch. Black noted in his case illus- 
trated, a covering of squamous epithelium upon the periphery of the 
growth, which might be interpreted as the transformation of meso- 
blastic into epiblastic tissue, but the correct explanation beyond 
doubt is that advanced by the same author, that the epithelium is 
transplanted from the gums, and grows after the manner of a skin 
graft. The growth does not contain nerves. The cavity in which it 
lies is often fairly free from decalcified dentin, the walls appearing as 
though subjected to an absorbent action. 

These growths may undergo further changes; higher organization 
of the granulation tissue occurs and fibrous tissue is formed; the cells 
may undergo degenerations, first granular, then fatty, and suppura- 
tion and gangrene may occur. Tomes 1 records a case where calci- 
fication of an hypertrophied section of a pulp occurred; but as the 
case w T as due to traumatism (fracture of a tooth), different vital 
conditions existed from those in the cases under discussion. Actual 

1 Dental Surgery, third edition. 



504 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 



calcification of the mass is scarcely possible, although calcareous 
degeneration may occur within the fungous mass (Fig. 437, G). 

While the growth occupies a cavity of decay, it seems at times to 
have acted upon the carious dentin so as to remove it by absorption, 
leaving the cavity more or less clean. 

Fig. 437 




Hyperplastic myxomatous pulp, which filled a carious cavity: M, lobules made up 
of papillae of a myxomatous structure, rich in capillary and venous bloodvessels; G, 
calcareous globule; E, epithelial cover of papillae. X 10. (Bodecker.) 



Resorption of the walls of the pulp chamber may occur as an 
accompaniment of chronic pulpitis. What appears to be an idio- 
pathic dentin resorption is described on p. 487. Black records a 
case where, after pulp capping in a lower molar and the insertion 
of a large gold filling, the tooth was examined at the end of ten years; 
for two or three years the pulp had given evidences of irritability, 
and when the pulp was removed the pulp chamber was found enor- 



CHRONIC INFLAMMATION OF THE PULP 



505 



mously enlarged and opening into the pericementum between the 
roots of the teeth. Fig. 438 exhibits resorption of previously formed 
secondary dentin with the probable agency through which the 



Fig. 438 



Sp-A' 




Acute pulpitis: S, secondary dentin; B, bay-like excavations filled with medullary 
or inflammatory corpuscles; V, transverse section of a bloodvessel; M, multinu clear 
body. X 300. (Bodecker.) 

resorption is brought about. The area of resorption is invaded by 
numerous multinucleated cells, which are evidently performing the 
function of odontoblasts. 



Fig. 439 



Fig. 440 



Fig. 441 



Fig. 442 




Hypertrophy of pulps. (Garreston.) 



As shown by Miller, Hopewell-Smith, and others, a reconstructive 
change may occur and adventitious dentin be redeposited in the 
area of resorption (Fig. 422). 

Symptoms. — The symptoms of chronic pulp inflammations and 
degenerations are usually those of long-continued discomfort, with 



506 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

reflex pains, which rarely persist into the latest stages of degeneration. 
The response to heat and cold, present at first, declines until the 
pulp scarcely reacts, and then but slowly. 

No nerve fibres develop in the hypertrophic pulp tissue, so that 
the newgrowth has no sensitivity in itself, although pressure upon it 
may cause sharp pain through the still vital pulp nerves themselves. 

Four or five of these hypertrophies may exist in a mouth, filling 
whole cavities of decay, the surrounding tooth structure being in 
various stages of disintegration. They seem to be comparatively 
insensitive to mastication (Fig. 440). 

Fig. 443 Fig. 444 








Hypertrophy of the gum. Hypertrophy of the pericementum. 

(Garretson.) (Garretson.) 

Hypertrophy of the pulp also may be associated with pulp ulcera- 
tion, the growth arising from one canal of a tooth. 

Regeneration of an extirpated pulp has been claimed. These are 
probably referable to the above form of hypertrophy, or to a fungoid 
growth from the pericementum or supposed extirpation under cocaine. 

Diagnosis. —The only condition with which hypertrophic pulp may 
be confounded is a pedunculated growth of gum tissue through a 
cavity at the neck of a tooth beneath the gum margin, or through 
a perforation either accidental or by caries (Fig. 444). It is impor- 
tant to differentiate between these conditions, because, if an appli- 
cation of arsenical paste be made to a fungous gum, the destruction 
of tissue may extend into the sound pericementum. The physical 
appearances of the two are alike; they both bleed freely and have 
about the same degree of sensitivity. 

Histological examination of this class of hypertrophy of the gums, 
conducted by Dr. Luigi Ancone, 1 of Italy, demonstrated that the 
growth is a simple exaggeration of the normal elements of the part. 

If the tumor be central to the tooth tissue and the latter not 
decayed out to very thin walls, it may be at times laid aside by means 
of a blunt instrument and be seen to have its origin from an orifice of 
exposure (Fig. 439). As a rule, a hyperplastic pericementum will 

1 Abstract from l'Odontologia, by Dr. W. Dunn, in International Dental Journal, 1899. 



CHRONIC INFLAMMATION OF THE PULP 507 

be found to have its attachment much lower or more lateral than 
a hyperplastic pulp, and the pulp cavity be seen to have been enlarged 
by caries, even more than shown in Fig. 362. It is then fairly inferred 
to be a gum mass, especially if the tooth has never been operated 
upon. The diagnosis may be a doubtful one, in which case the 
rubber dam is to be applied, the polypus frozen by means of a spray 
of ethyl or methyl chlorid, and the mass removed with a sharp 
blade passed across its peduncle. The electric cautery may be used 
to ablate the mass. 

The source of the tumor may then be usually clearly seen. As an 
alternative proceeding the tissue may be thoroughly saturated with a 
strong solution of trichloracetic acid and then ablated. If any fur- 
ther doubt exist, the pulp is to be sterilized with hydrogen dioxid, etc., 
and a pellet of cotton saturated with oil of cloves, carbolic acid, or 
dental tincture of iodin is laid upon it, and over this temporary stop- 
ping is firmly packed. By this means the growth may be pressed 
away until it is seen to arise from either a pulp chamber or a perfora- 
tion made by decay or accidental excavation into the pericemental 
tract. 

Pressure anesthesia may be resorted to partly as a diagnostic 
measure. In such case no danger exists beyond the possible forcing 
of cocain into the gum tissue. Nervocidin should be useful in cases 
of doubt. Skiagraphy should afford a diagnosis. Hemorrhage may 
be checked with alum and thymol in powder or solution, or by the 
use of trichloracetic acid, silver nitrate, zinc chlorid, or iodin. 

Treatment. — If the case be one of pulp hypertrophy, arsenic may 
be applied or pressure anesthesia attempted for pulp removal. 

Crystals of iodin have been used with satisfaction in combination 
with pressure for pulp devitalization. 1 If a perforation exist, it is to 
be treated by sealing the orifice with gutta-percha, copper amalgam, 
or oxyphosphate of copper cement. (See p. 561.) 

Infarction of the Pulp. — The production of infarction may result 
as described under Fibroid Degeneration, and as described consists 
of minute circumscribed hemorrhages from end arteries into the pulp 
tissue. This differs somewhat from a true infarction. (See p. 119, 
and Fig. 445.) 

Fibroid Degeneration of the Pulp. — Apart from the degenerations 
due to inflammatory conditions, a form of degeneration occurs "as a 
natural old-age termination of the life of a healthy pulp, and similar 
tb senile changes occurring in the pericementum." (See Fibroid 
Degeneration of Pericementum). This change, as described by 

1 Truman. 



508 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 



Hopewell-Smith, 1 occurs in teeth of the aged in whose mouths simple 
alveolar resorption has occurred, though later he 2 has shown that it 
may occur in the pulps of young persons, in sound teeth extracted 
for irregularity, and even in teeth in which the dentinal wall or pulp 
cavity is not completed to a typical calcification. He regards it 

Fig. 445 




H, hemorrhagic infarct; R, rupture of bloodvessel; D, dentin; 0, vacuolated odonto- 
blasts; F, early fibrosis of pulp. X 250. (Hopewell-Smith.) 

as due to a primary thrombosis of the capillaries and veins, with 
permanent dilatation of the arteries, with or without tiny hemor- 
rhages, the lack of collateral circulation and lymphatics con- 
tributing to the atrophy. As a cause he suggests chemical change 
in the blood through systemic derangement, as anemia, chlorosis, 
or exhaustive diseases, the red corpuscles being fewer and the 



Histology and Pathohistology of the Teeth. 



Dental Cosmos, 1907. 



CHRONIC INFLAMMATION OF THE PULP 



509 



leukocytes and blood platelets increased, thus favoring a thrombosis 
of small vessels; also, that here inflammatory changes in the peri- 



DO 



Fjg. 446 




Horizontal section of fibroid degeneration of the pulp in situ. Prepared by Mr. 
Hopewell-Smith's process: D, deeply stained dentin; S, large areollar spaces; DO, 
degenerate odontoblasts; P, fibroid tissue of pulp. X 45. (Hopewel-Smith.) 



cemental tissue might interfere with the pulp circulation sufficiently 
to produce it. 



510 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 



Clinical Significance. — While the form of thrombosis or fibrosis 
may not be diagnosticated because of lack of related symptoms, 
Hopewell-Smith argues that they should be suspected in weak and 
unhealthy patients, and that such suspicion should contra-indicate 
conservative operations, also that they may explain certain difficulties 
of devitalization or anesthetization of the pulp or cause a related 
change in the pericementum or brittleness in the dentin. 

Fig. 447 



P™ 



D 




-FO 



Fibroid degeneration of the pulp: D, dentin with tubules; FO, fibroid odontoblasts; 

P, atrophied pulp tissue. 



Morbid Anatomy. — "The odontoblasts become sheaved with or 
without fatty degeneration; the arteries, permanently distended, 
undergo hyaline degeneration; a reticular atrophy occurs, with dis- 
appearance of cells and nuclei of both pulp and vessels and nerves, 
and, at the same time, the connective-tissue fibres undergo hyper- 
plasia. The pulp goes more or less gradually through the stages 
shown in Fig. 445, finally producing the stage shown in Figs. 446 
and 447, in which the pulps are shrunken and may have left the wall 
of the pulp chamber. "Many areolar spaces appear which may be 
arranged in chains. The odontoblasts are degenerated. The pulp 



CHRONIC INFLAMMATION OF THE PULP 



511 



stroma is very dense, has a clear, fibrous structure, becomes very 
marked in staining, and is highly differentiated from the surrounding 
tissue. The bloodvessels, nerves, cells, and connective-tissue have 
all disappeared, and their place is taken by a new, firm, fibrous 
structure devoid of cells, nuclei, or any regular arrangement of 
constituent parts." 

Fig. 448 




Fatty degeneration of the pulp. (V. A. Latham.) 



"There is no calcification of the pulp and no obliteration of the 
dentinal tubules. 

" The proximate cause and associate phenomena are not as yet 
clearly related." 

Fatty Degeneration of the Pulp. — During the course of degenera- 
tion of the elements of the pulp fatty changes may occur as in other 
parts. The fatty changes occur in the walls of the arteries and 
sheaths of the nerves, and in the odontoblasts. (Hopewell-Smith.) 

Cloudy swelling also appears. (Latham.) (See Fig. 512.) 



512 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 
Fig. 449 




Cloudy swelling; parenchymatous degeneration; pulp nodules. (V. A. Latham. 1 ) 

Fig. 450 




Colloid degeneration of_the pulp. Compare with Fig. 49. (V. A. Latham.) 

1 Dr. Vida A. Latham's illustrations are from her paper on Some Pathological 
Features of the Pulp, Journal of the American Medical Association, September 22, 
1906. 



CHRONIC INFLAMMATION OF THE PULP 
Fig. 451 



513 




Great thickening of nerve bundle. From a case of chronic neuralgia. Patient had 
many teeth extracted for neuritis. (V. A. Latham.) 

Fig. 452 




33 . 



Neoplasm of the pulp. (V. A. Latham.) 



514 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

Colloid Degeneration of the Pulp. — The demonstration of colloid 
material within the pulp has been made by Latham, as shown in 
Fig. 450. She states that it may become calcified. The condition 
is very rare. Other degenerations such as Wallerian, hyaline, and 
amyloid have been noted. 1 It would seem that the pulp may be 
subject to any form of degeneration seen elsewhere. 

Nerve-end Degeneration of the Pulp. — The degeneration of nerves 
occurs in the pulp as it may in the pericementum and from the 
same causes that produce endarteritis. The bundles may be enlarged. 
Neuralgia may be associated with it. 

Neoplasm of the Pulp. — Latham claims that a neoplasm may occur 
in the pulp, and offers the photomicrograph shown in Fig. 452 as 
proof of the fact. I do not know of any cases in which such a pulp 
condition has been related with a malignant growth outside of the 
pulp cavity, though it may not be impossible. 

Many of the destructive pulp diseases occur in the pulps of the 
temporary teeth, and are to be treated in like manner, except as to 
the use of arsenic, which, being accompanied by greater danger, 
should, for the most part, be replaced by other methods of pulp 
removal. This point is discussed at length in the chapter upon 
Removal of the Pulp. 

If the tooth roots be largely resorbed, the pulp may bear capping 
even when ulceration has occurred. The pulp may die under this 
capping, when the case is further treated as indicated. (See Chronic 
Apical Abscess.) 

1 Talbot: Dental Cosmos, 1909, p. 1150. 



CHAPTER XVII. 

METHODS OF REMOVAL OF THE DENTAL PULP 
AND ROOT-CANAL FILLING. 

There are four general methods by which a patient or pulp may 
be prepared for the operation of pulp extirpation. These are as 
follows : 

1. Anesthetization of the patient and removal of the pulp during 
the period of anesthesia. 

2. Anesthetization of the pulp by cocain or novocain, or in some 
cases by nervocidin, and the removal of the pulp. 

3. Anesthetization of the apical tissue with novocain by the mucous 
or conductive method and removal of the pulp. 

4. Devitalization of the pulp followed by its removal. 

1. General Anesthesia. — The pulp of a single-rooted tooth may be 
readily extirpated while the patient is anesthetized by nitrous oxid, 
nitrous oxid and oxygen, or by somnoform. The instruments should 
be in readiness, the patient anesthetized, the pulp uncovered by 
an engine bur, and the pulp extirpated with a barbed broach or 
Donaldson cleanser. 

In cases of multirooted teeth the available anesthetics are ether, 
which is' rarely used for the purpose, and nitrous oxid and oxygen 
administered by nasal inhalation. The latter is accomplished by 
means of a special apparatus having a hood covering the nose, or 
bulbs entering the nostrils. This is designed to prolong the anesthesia 
by administering nitrous oxid and oxygen. As it is equally appli- 
cable to the excavation of cavities of decay and extractions, it is 
a valuable means for this purpose. (See p. 398.) 

The ordinary outfit is, however, of value by enabling the operator 
to remove the diseased bulb of the pulp of a multirooted tooth, after 
which and while the patient is conscious other methods of removal 
of the radicular portions of the pulp may be employed. (See p. 491.) 

2. Anesthesia of the Pulp. — For this purpose cocain hydrochlorid 
or novocain are employed. There are three practical methods by 
which it may be introduced into a pulp : 

(a) By pressure accomplished by means of raw vulcanite. A strong 
solution (50 per cent, to saturated solution) of cocain hydrochlorid 
or novocain is made in water, or preferably in some mild antiseptic 

(515) 



516 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

solution which does not cloud on admixture (as Borine) A small 
piece of amadou (spunk) is saturated with it and laid upon the orifice 
of exposure. The cavity is filled with the rubber, and upon this is 
placed a flat-ended plugger or burnisher broad enough to concentrate 
the force upon the amadou. A broad piece of amadou placed over 
the rubber is sometimes of assistance in preventing the slipping 
about of the rubber. Gentle pressure is now made and a slight pain 
is usually felt. The pressure should be maintained until this passes 
away, then it is increased little by little until some force is exerted. 
The rubber and amadou are then removed, the pulp cavity opened, 
the progress of the anesthesia tested with a fine broach, and the pulp 
lifted away. Some prefer to place a prepared pellet of cocain or 
novocain upon the pulp. 

For multirooted teeth the pressure should be prolonged, and to 
prevent return of sensation and hemorrhage while extirpating it is 
well to instil carbolic acid into the pulp tissue by means of a fine, 
smooth broach. 

In some cases the operation fails because the direction of the 
pressure has been away from the pulp or because the spunk has 
slipped from its place. Sometimes the orifice of exposure may be 
enlarged, but as sensation is discovered a fresh application must be 
made. In cases with large foramina the application may fail; with 
the incomplete foramen of moderate size it is more successful. 

Sometimes repeated applications fail to effect, though the appli- 
cation is not painful, and at times the pressure is not tolerated at 
all, owing to the irritability of the pulp, due to continued hyperemia 
or inflammation. Even six or eight applications have at times 
failed even when a fair and accessible exposure existed. Sedation 
for a day or two sometimes permits a successful application. The 
pressure is sometimes tolerated, yet failure results. This action of 
cocain corresponds to that in inflamed tissue. Sometimes, even 
when the spunk enters the pulp tissue, the pulp is still sensitive 
higher up. In such a case I have often packed devitalizing fiber 
into the pulp in place of the spunk and without further pain. In 
cases of cavities without walls to confine the rubber, it is well to 
enclose the buccal and lingual embrasures with the thumb and 
forefinger. In very broad occlusal cavities the finger-tip confines 
the rubber nicely. 

When only canal filaments are present, any septic matter present 
should be removed by syringing repeatedly with an antiseptic solu- 
tion; then the canals should be thoroughly dried, and the cocain, 
dissolved in an antiseptic, is carried on a cotton thread into the canals 
and against the pulp remnant. A small piece of rubber is placed in 



ANESTHESIA OF THE PULP 517 

one canal and the pressure confined to that canal by means of a 
plngger which will about fill the canal. The action is then repeated 
in the other canals. This produces better results than a general 
pressure over all the canals at once. 

If used after arsenic has been applied the results are not usually so 
good, but sometimes the method is successful. To avoid the intro- 
duction of arsenic into apical tissue all sloughing portions should be 
removed and all arsenic washed out. 

When the pulp is not exposed, the application to the dentin over 
the pulp permits advance, a pocket being created in the dentin with 
a bur, which aids the further instillation of the cocain; finally, the 
pulp is exposed and the anesthesia is completed. 

Clyde Davis recommends for the purpose of producing the exposure 
the use of a drop of 1 to 1000 adrenalin chlorid followed by a drop of 
37 per cent, formaldehyd, then pressure with raw vulcanite. 

'Where calcific formations are present they present some difficulty, 
though with persistence one may be enabled to anesthetize the pulp. 
Custer recommends 75° to 90° sulphuric acid to aid in loosening 
the nodule. Cook recommended an application of 10 per cent, 
sulphuric acid for a few T minutes, followed by sodium bicarbonate 
previous to a reapplication of the pressure anesthesia, as highly 
effective in aiding penetration of the cocain. Desiccation is always 
a valuable preliminary, aiding penetration. Claims are made for 
eucain, or alcohol for producing pulp anesthesia by pressure. 

There is a possibility of the introduction of cocain into the general 
circulation, and some systemic effect may be noted, though often 
this will 'be due to the agitation of the patient. Some patients have 
complained of tingling in the fingers. If syncope be threatened 
aromatic spirit of ammonia should be administered, the head lowered, 
the feet elevated, and smelling salts or amyl nitrite applied to the 
nostrils. It is always well to administer aromatic spirit of ammonia 
or camphorated validol before using cocain for any purpose. 

Hemorrhage following the extirpation of the pulp is sometimes 
copious. To avoid this, carbolic acid should be instilled into the 
pulp tissue by means of a smooth broach. A fine Donaldson cleanser 
may be passed to the apex of the canal and slowly twisted, the oper- 
ation consuming several minutes. This torsion of the pulp largely 
limits the hemorrhage. If it occur it should be allowed to check 
itself, though if desired a trifle of a mixture of powdered alum and 
powdered thymol may be taken upon cotton wet w^ith phenol- 
camphor and passed to the end of the canal. Deliquesced zinc chlorid 
checks hemorrhage promptly; a dilution is less painful. 

It is an open question whether canals from which living pulps 



518 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

have been removed should be filled immediately or not. There is 
liable to be a secondary hemorrhage, particularly when adrenalin 
is used with the cocain. Many prefer to fill at once, claiming that 
surgical pericementitis is the only result. The writer, as a rule, wraps 
a twist of cotton upon a Swiss broach, dips it into phenol-camphor, 
then into formocresol, and applies it to the canal. This, as a rule, 
permits the healing of the parts without much tenderness, and 
really consumes but little more time in the aggregate. Moreover, 
the formocresol tends to mummify the fibrils left in the dentinal 
tubules. 

All work should be done under aseptic precautions. Where applic- 
able and not liable to be too painful, the rubber dam should be 
applied. The writer often uses napkins instead, and relies upon the 
carbolic acid instilled into the pulp and the formocresol dressing to 
maintain asepsis. This is repeated if the cavity be douched out. 

(6) When considerable dentin overlies the pulp, or when a tooth is 
sound, the most expeditious method of pulp anesthesia is by means 
of the compound syringe. This consists of a strong metal syringe, 
the piston of which is actuated by means of levers which multiply 
the power of the hand. The Myers syringe is one of the best, 
though several forms are obtainable (see Fig. 375). The syringe 
nozzle is embedded in a small hole drilled in the dentin by one of 
two methods : The hole may be made small with parallel sides, as 
when drilled with a No. \ bur; the syringe nozzle has then slightly 
conical sides at the point, intended to jam a fit when introduced with 
force into the drill pit. In the other method the drill pit is made 
with a cone-pointed bur or bud bur, and the syringe point is made 
flat-ended, a form easy to maintain upon the point. A 4 to 10 per 
cent, novocain solution is sufficient, and all air must be expelled 
from the syringe. It is wise also to expel all air from the drill pit 
by a slight pressure while the syringe point is loosely held in the pit. 
Then a rotary motion under forward pressure embeds the point. 

If no leakage occurs the force of the piston drives the anesthetic 
through the fibrils in the tubules and into the pulp. The pressure 
must be maintained for about three minutes. The anesthesia is 
then tested by drilling with a No. \ bur in the direction of the pulp. 
If the dentin be sensitive the syringe is to be reapplied. Often the 
bur sinks into«a sensitive pulp without warning by dentinal sensi- 
tivity. In such case the syringe is reapplied for a moment, when, 
as a rule, the anesthesia will be complete. In all cases when testing 
the drill hole should not be enlarged, as this prevents reapplication. 
Too much cocain should not be introduced, as it has happened that 
the area about the apical tissue has been profoundly injected, with, 



ANESTHESIA OF THE PULP 519 

of course, possibility of systemic complication. This warning 
applies to the second application rather than the first. Novocain is 
less dangerous. When desirable, the enamel of a sound tooth which is 
to be crowned may be ground away until the dentin is reached, or 
if enamel must be removed in only limited degree, as for a tap upon 
the lingual side of an incisor or in the fissure of a bicuspid, a "spot" 
is first made with a dentate bur, then a spear drill is driven through 
the enamel only just reaching the dentin. The drill hole is then 
enlarged as widely as permissible, after which the pit is made in the 
dentin with a Xo. § bur. 

The lingual side of upper incisors will permit of sufficiently direct 
pressure to enable the operator to centre the syringe point, but in 
many cases in which crowns are indicated the labial side may be 
used with advantage, especially at the neck when the cementum is 
exposed. Later, the entrance tap is made in line with the pulp axis. 
The labial or mesiobuccal side must always be used in the lower teeth, 
unless a cavity be used, sometimes preferably at the neck, sometimes 
higher up. In cavities having sufficient dentin over the pulp the pit 
may be made in the pulpal wall, and if for any reason it is needed 
the drill pit may begin at the cervical portion of the cavity and extend 
into the root dentin and parallel with the pulp. The pit must be 
deeper than the syringe point will penetrate, so that the pressure 
may force the solution laterally through the tubules, which are at 
a right angle to the axis of the pulp and the pit. In some cases solu- 
tions of antiseptics have been as effective with this instrument as 
the cocain solution. The experiment may not be successful. 

According to Brouardel, 1 of Paris, the effects of cocain are acute 
and chronic. The former develop usually in ten or fifteen minutes, 
or even up to three-quarters of an hour after the injection. They are : 
precordial anxiety, filiform and extra rapid pulse, lividity of the face, 
coldness in the extremities, and abundant perspiration; rise in tem- 
perature, irregular respiration, tingling sensations in the hands, 
blunted tactile sensibility, excitement, loquacity, weeping, anger or 
hysterical fits; bilious vomiting with or without diarrhea, anuria, 
symptomatic epilepsy, followed by motor and sensory paralysis. 
Death occurs in from two minutes to five hours after administration, 
though in the chronic cases fatality usually does not result. 

Placing the patient in the horizontal position, give inhalations 
of amyl nitrite, and, if further cardiac stimulation be necessary, 
hypodermic injections of ether or strychnin. 

The chronic poisoning occurs mostly in those addicted to its use. 

1 Dental Cosmos, 1905, p. 1508. 



520 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

Some develop a tolerance of the drug, withstanding from 30 to 120 
grains. Tachycardia and intense psychic disturbances, leading to 
physical and mental collapse, are observed. 

(c) The third and least desirable form of cocain anesthesia of the 
pulp consists of its introduction by the cataphoric current. It has 
the disadvantage of consuming more time, but may serve when 
patients are timid. A 10 per cent, solution of cocain hydrochlorid 
is applied to the pulpal wall of the cavity, the tooth being previously 
placed under rubber dam. The anode of the cataphoric outfit is 
applied to the cotton and the cathode placed in the hand or at the 
cheek. 

The dentin may be anesthetized as well. If desired, this method 
may be used to obtain a pulp exposure and the pressure method 
employed to complete the operation. 

When beginning with an exposed pulp, about fifteen minutes will 
be required unless hyperemia of the pulp exists, when a longer time 
will be required. As with the pressure method, there may be occa- 
sional failures. It will be noted that there is advantage in time and 
convenience in the pressure methods. (See p. 403.) 

(d) The fourth method of producing pressure anesthesia consists in 
the use of carbolic acid in place of the cocain, or in case of obstinate 
canal filaments of a solution of cocain in carbolic acid. (See p. 496.) 

(e) The fifth method of producing pulpal anesthesia is by the 
application of nervocidin, an alkaloid obtained by D. Dalma from 
the East Indian plant gasu-basu. Arkovy recommended that a 
portion be applied to the exposed pulp for twenty-four hours, when 
it may be removed painlessly. Soderberg 1 suggests the addition of 
a small amount of cocain hydrochlorid to overcome the primary 
irritating effect of the nervocidin. If dentin be over the pulp, an 
additional application of twenty-four hours' duration is required to 
obtain an exposure. (See p. 409.) 

Sprays of rapidly vaporizable substances, such as ethyl or methyl 
chlorid, directed against the exposed pulp, the tooth being isolated 
under rubber dam, will, in some cases, render the pulp entirely 
insensitive, although, as a rule, they fail to entirely anesthetize to 
the apical foramen. The method is painful and not applicable in 
many cases of highly irritable pulps. (See p. 402.) 

3. Anesthesia of the Conductive Apparatus. — The third general 
principle consists in the use of mucous, diploeic or conductive 
anesthesia to block the transmission through the fifth nerve leading 
from the part. This has been previously described for hypersensitive 

1 Dental Cosmos, 1901 and 1902. 



DEVITALIZATION OF THE PULP 521 

dentin (see page 407). Claims have been made for a slight sidewise 
blow struck upon the tooth to paralyze the pulp nerves by a stretch- 
ing shock. 

4. Devitalization of the Pulp. — Devitalization of the pulp by the 
use of arsenic trioxid as a preliminary to its successful removal 
is the oldest of the methods employed at the present day, 1 and 
as shown, it still has to be resorted to either from necessity or 
convenience. 

The method has its value in the very teeth in which its use is least 
objectionable, namely, the posterior teeth. There is no danger of 
the use of arsenic in teeth having completed roots, or in unresorbed 
temporary teeth, provided the arsenic be accurately sealed in the 
cavity so that it does not escape upon the gum. If it does escape it 
may destroy the gum or pericementum and cause partial necrosis of 
bone or the complete loss of the tooth together with some bone. The 
pulp always dies through a process of venous hyperemia induced by 
the protoplasmic irritant and poison. Some of this is absorbed by 
the pulp. This hyperemia is progressive from the pulp bulb toward 
the apex of the root, and there it causes the death of the apical portion 
of pulp through interference with its nutrition. Sometimes this 
hyperemia of the pulp extends into the apical tissue, but if the pulp 
be left in situ, necrosis of apical tissue never results, but, on the 
contrary, the hyperemia becomes resolved after the death of the 
pulp. 

The writer fails to see wherein such a hyperemia differs in conse- 
quence from that produced by the surgical removal of a pulp and 
denominated with favor as surgical pericementitis. In his hands 
such teeth have given quite as good results as when other methods 
have been employed. By this it is not meant that there has been 
no difficulty in devitalizing some pulps, particularly some of those 
in which repeated applications of cocain under pressure failed to 
anesthetize, but that when carefully handled and sufficient time for 
pulp death has been allowed, careful filling of the canal has been 
successful. 

Action of Arsenic upon the Pulp. — Arkovy 2 was the first to point 
out the details of the action of arsenic upon the dental tissues : 

"1. As 2 3 brought into contact with the tooth pulp acts in the 
following way : A certain degree of inflammatory hyperemia, total or 
partial, depending upon the quantity of the agent applied, sets in; 
the bloodvessels become expanded, and here have a tendency to 
thrombosis. This latter effect may also be in connection with 

1 Introduced by Spooner in 1836. 

2 Transactions of the International Medical Congress, London, 1881. 



522 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

embolism of the capillaries, when the agent is quickly taken up into 
the bloodvessels. 

"2. AS2O3 produces no coagulation of tissue whatever. 

"3. It has a specific influence upon the blood corpuscles, combining 
with the hemoglobin to form a compound of arsen-hemoglobin, and 
of this chemical process there seems to be evidence in the profuse 
yellowish tinge of the whole pulp tissue and in the discoloration of 
blood in several of the bloodvessels. 

"4. In nearly every case it is taken up in substantia (in form of 
molecules) into the blood-ways; when there it produces besides the 
above-mentioned changes, granular detritus of the contents and 
anemic collapse — shrinkage, the latter effect being brought about 
nearly exclusively in cases where greater doses were used. 

"5. The bulk of the pulp tissue — viz., connective-tissue fibers and 
odontoblasts — undergoes no change whatever; not so the connective 
tissue cells, which increase three or four times their normal size. 

"6. The special action of arsenic trioxid upon the nerve element 
consists in the following: the neurilemma is only so far influenced 
that its nuclei are somewhat increased; a more essential change takes 
place in the axial part, where, after the application of more than 
1 mg., granular destruction of myelin sets in, and the axis-cylinder 
commences here and there to disappear. A very surprising alteration 
may be seen in the notchy tumefaction of the axis-cylinder, described 
heretofore almost only in cases of central lesions. 

" 7. All these alterations occur in and among normal-looking tissue. 

"8. The action of arsenic trioxid is macroscopically exhibited by 
a brownish-red tinging of the whole or of certain parts of the pulp 
body, as well as of the neighboring dentin and the cementum, this 
latter in cases treated with greater doses — viz., 2 to 5 mg. This 
alteration is most expressed at the top of the crown pulp and at 
the apical one-fourth to one-third part. This circumstance may 
be considered as an external evidence of the devitalization being 
completely attained to." 

In some cases the pinkish discoloration of the dentin may be 
marked; the broken-down corpuscles of the extravasated blood have 
their coloring matter taken up by the odontoblasts, and being dis- 
tributed through their protoplasmic processes produce a condition 
technically known as suffusion. The same result may be an attendant 
upon injury to the vessels from other causes, producing hyperemia, 
as when teeth are moved too rapidly in regulating. (See p. 480.) 

Miller's experiments 1 upon the tails of mice (made without and 

1 Dental Cosmos, 1894. 



DEVITALIZATION OF THE PULP 523 

with rings at the root of the tail to simulate the surrounding of the 
apical vessels of a tooth; made without and with encasement of the 
tails in plaster of Paris to imitate the rigid surroundings of the dental 
pulp) showed that in the absence of the plaster encasement enormous 
edema of the tail was produced and a sensory paralysis of the hind 
limbs; complete anesthesia of the tail occurred in forty-eight hours. 
" The action of arsenic appeared somewhat accelerated when a glass 
ring was applied close to the root of the tail. In more than forty cases 
there was not one in which the action of the arsenic extended beyond 
the ring, and the action was not appreciably affected by enclosing the 
tails in plaster casts. The action of the arsenic is of a progressive 
nature, beginning at the point of application and extending gradually 
in each direction." 

Flagg 1 devitalized ten pulps and removed them, cut off the portion 
of the bulb of each which had contact with the arsenic, and tested the 
ten pulps together by Reinsch's test. Arsenic was found, estimated 
at a one-hundred-thousandth part of a grain, or one-millionth of a 
grain for each pulp. Allowing for possible mechanical introduction 
or contact of arsenic during extirpation, the quantity of arsenic 
introduced by the circulation must be very minute indeed. 

Flagg argued that as the pulp subsequently putrefies it cannot 
have died as the result of arsenical poisoning alone. 

In the roots with large foramina arsenic may be absorbed, as areas 
of devitalization of the apical and overlying gum tissue have been 
noted. In several apparently authentic cases the pericementum of 
a mature tooth has been said to be destroyed from the apex down 
and the tooth lost. I have never seen such a case resulting from the 
arsenical method alone in either clinical or private practice, although 
cases of marginal gum, alveolar, and pericemental death, beginning 
as the result of leakage or application to perforations, have been 
noted. It is probable that as stasis proceeds the apical portion of 
the pulp becomes involved in advance of arsenic absorption. Miller's 
experiments show that arsenic does not pass the point of constriction. 

Variations in the Action of Arsenic. — In most cases of fully formed, 
single-rooted teeth in young adults an application of arsenical paste 
directly to the exposed pulp will be followed by the complete death 
of the organ in forty-eight hours. At the expiration of that time a 
sterilized broach may be passed almost to the apex of the root and 
the pulp removed en masse without pain. Pulps of molars require a 
longer time, often a week, before the filaments are dead. The finer 
filaments resist longer than the larger ones. If pulp nodules exist, 

. * Dental Cosmos, 1868. 



524 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

the action of the arsenic may be delayed or in some cases be almost 
nil. In calcareous and other chronic pulp degenerations the action 
is also delayed. If arsenical applications are made over a layer of 
dentin, the same delay is noted, and is increased in very dense 
teeth. There is also a greater tendency to suffusion. 

Some pulp, irrespective of the pulp condition, exhibits a peculiar 
idiosyncrasy in resisting the action of arsenic, requiring large doses 
and long applications before succumbing. Second applications often 
require more time to kill the balance of the pulp than the first appli- 
cation would have required. The time used in investigation is 
practically lost. The editor, therefore, allows plenty of time; about 
ten days for molars, five for single-rooted teeth, and prefers to find 
the pulp entirely dead. 

The rational objections to arsenic, aside from its escape upon the 
gum, are: (1) The possible production of pain. (2) Possible suffu- 
sion of the tooth. (3) The time required. 

The production of pain may largely be obviated by observance of 
certain technique. The pulp should ordinarily be exposed and be 
slightly bled to relieve any hyperemia or inflammatory engorgement 
present, as this seems to prevent the absorption of the arsenic, A 
powerful sedative, such as thymol, menthol, cocain hydrochlorid 
or morphin acetate, should be employed as a corrective, and the 
menstruum should be sedative rather than coagulant. All pressure 
on the pulp should be avoided as this produces pain. 

Sufficient time for complete death should be allowed, say, from a 
week to ten days. If, upon examination with a fine smooth broach, 
vitality be discovered, a sedative should be applied and pulp death 
awaited. Leaving the dead portion against the vital part of the pulp 
is even better than making a second application, as its removal 
relieves the congestion by opening the vessels, and the congestion is 
necessary to the end in view. If the pulp give but little response 
upon probing it may be removed. Sometimes the diapedesis of red 
corpuscles, associated with the venous hyperemia, causes a staining 
of the pulp and dentinal fibrils with the liberated hemoglobin. This 
is unfortunate, but can be treated by bleaching with 25 per cent, 
ethereal pyrozone sealed in the pulp cavity for about twenty-four 
hours after the pulp is removed. The third objection, the matter 
of time, does not apply to the cases of prompt devitalization, as the 
time spent in pulpal anesthesia and checking hemorrhage is in the 
aggregate no less than in the arsenical cases. In the delayed action 
of arsenic the objection is valid, but the conductive and general 
anesthesia methods are still open to trial. The arsenical method, of 
course, requires a longer period of treatment. Pulpal anesthesia 



DEVITALIZATION OF THE PULP 525 

can be tried when arsenic does not act well, but should be avoided 
when it originally failed. Mucous, diploeic and conductive anesthesia, 
or general anesthesia may be used if arsenic fails. As stated, these 
considerations apply mainly to posterior teeth. 

Forms in Which Used. — The following is an excellent formula for 
arsenical paste: 

1$ — Arsenici trioxidi gr. xv 

Cocainae hydrochloridi gr. xx 

Thymolis (vel mentholis) gr. v 

Olei caryophylli q. s. ft. pasta — M. 

This should be finely ground in a mortar and spread over the bottom of a wide glass 
jar so that some of the paste may be taken up from the bottom. The arsenic settles 
to the bottom. 

Buckley recommends the following formula: 

1$ — Arsenic trioxid gr. clxxx 

Cocain alkaloid gr. xxx 

Thymol gr. xv 

Petronal lUxv — M. 

Either of the above may have the powdered ingredients mixed. 
The cotton pellet may be w T et w T ith the menstruum and then dipped 
into the powder. Lamp black added to the paste colors it so that it 
is easily distinguishable in a cavity. 

Prinz has suggested the rational improvement of using a con- 
centrated solution of cocain or novocain before applying arsenic. 
This renders its primary action less painful, or painless. 1 

The following are other formulae: The analgesics included are 
intended to dilute the arsenic and quiet the pulp, and thus both 
directly and indirectly modify the pain. 

J£ — Acidi arsenosi, 

Morphinse sulph aa gr. x 

Acidi carbolici q. s. ft. pasta — M. 

(J. D. White.) 

1$ — Acidi arsenosi gr. x 

Morphinse acetatis gr. xx 

Olei caryophylli q. s. ft. pasta — M. 

(J. Foster Flagg.) 
Creosote may be substituted for oil of cloves. 

Bf — Acidi arsenosi gr. x 

Cocainae hydroch gr. xx 

Olei cinnamomi q. s. ft. pasta — M. 

(E. C. Kirk.) 

1$ — Arsenic gr. x 

Alum gr. x 

Thymol gr. x 

Oil of cloves q. s. ft. pasta — M. 



Dental Materia Medica and Therapeutics. 



526 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

As the ordinary pastes tend to separate into layers of arsenic, 
morphin, etc., and menstruum if made thin, they should either be 
made into stiff pastes or spread over the bottom of a wide jar, so that 
some arsenic may be scraped off the bottom at each application. 

W. H. Truman indorses the opinion of J. D. White that 
thorough trituration for two hours more finely divides the arsenic 
and prevents separation, and claims that the use of arsenic 
triturated with wood creosote and glycerin is the most effective 
preparation. 1 

Miller offers the following general rules as deductions from his 
observations : 

"1. The rapidity and intensity of the action of arsenous acid 
depend, under certain circumstances, to a very considerable degree 
upon the substance or substances with which it is incorporated. 

"2. Where there is but a small point of exposure, and in particular 
where extensive calcification has taken place in the pulp, escharotics 
should be avoided, since the coagulation of the tissue retards the 
absorption of the arsenic. This retardation is but slight where there 
is a broad surface of exposure. In stubborn cases, where applica- 
tions of the ordinary paste fail to effect the devitalization, a paste 
consisting of arsenous acid in oil of cloves, glycerin, or salt solution 
should be employed, undiluted by any third constituent. 
.,"3. Thymol is worthy of a trial as a substitute for morphin, on 
account of its anesthetic and antiseptic properties. 

"4. For devitalizing pulps of temporary teeth or remains of pulp 
tissue in root canals, arsenous acid, if employed at all, should be 
diluted with two or three parts of some other constituent (thymol, 
zinc, oxid, morphin, iodoform). " 

Cobalt was introduced by Robert Arthur as a devitalizing agent 
some forty years ago. Within recent years it has been employed, 
notably by the Herbst method, to destroy pulps. The cobalt paste 
of Herbst was analyzed by E. C. Kirk, and found to consist of 
metallic arsenic and cocain hydrochlorid. Kirk suggests that free 
acids which cocain salts may contain, or the chlorin from the chlorid, 
may combine with the metallic arsenic and form soluble salts. The 
use of arsenic pentoxid and soluble arsenates has been suggested by 
Fette, and for which he claims advantages. 2 

There are some advantages in the so-called devitalizing fiber 
introduced by J. Foster Flagg. To make this, absorbent cotton is 
cross-cut with scissors to a fine lint. This is dusted into the paste 
or ground up with it in the mortar. It may then be dried on a blotter 

i Dental Brief, June, 1913. 2 Dental Cosmos, November, 1914. 



DEVITALIZATION OF THE PULP 



527 



Fig. 453 



and be bottled for use. As it lacks long fibers, a small portion may be 
detached and be placed upon the pulp. There are cases, however, 
in which the paste should be carried to the exposure upon a probe 
and gently inducted into a fine exposure. Here its tendency to spread 
or penetrate is valuable. The fiber has no such tendency, which 
makes it less dangerous in use. In making the application a minute 
portion of paste is to be laid upon the pulp, or a pin-head pellet of 
cotton is rolled in it, the excess of menstruum remoyed, and it is 
then applied to the pulp, or a portion of devitalizing fiber is used. 
This is then sealed in. 

The cavity should be prepared for the reception of arsenic, decay 
being removed as far as practicable, and the cavity dried. Any 
redundant gum must be pressed away or 
saturated with trichloracetic acid and 
ablated. 

There are two good methods of seal- 
ing the arsenic. In cases not approach- 
ing the gum, or where dryness can be 
maintained, the application may be 
accurately made and quick-setting cement 
flowed over it. This cement is capable 
of being fairly dropped into a cavity or 
led around the periphery by a probe, and 
should be very adhesive, also be readily 
removable. A still safer method consists 
in applying a pellet of amadou over a 
part of the pulpal wall. The cement is 
then introduced about the periphery of 
the cavity, the amadou being left largely 

uncovered. When hard, any cement over the amadou is removed 
and the latter lifted out, thus leaving a box-like receptacle for 
the arsenic and a pellet of amadou partly wet with eugenol in 
which menthol is dissolved. When placed, the orifice is dried and 
more cement added. This method of first making the covering is 
of special advantage when the cavity cervix is near the gum, and pre- 
vents the forcing of arsenic toward the gum in the act of making the 
covering. Amalgam or facing amalgam 1 or temporary stopping 
may be used in place of the cement (Fig. 453). Temporary stopping 
is not very safe against masticatory force. 

/The rubber dam is generally insisted upon, but cannot be used in 
the worst cases, hence an expert may dispense with it. There is a 




Diagram showing method of 
first making the covering for 
an arsenical or sedative appli- 
cation. (See text.) EP, ex- 
posed pulp; A A, arsenical ap- 
plication; C, sedative covering 
to same; A, amalgam placed 
before these applications; A', 
amalgam to seal them in; E. 
enamel. 



Facing amalgam is silver 40, tin 55, zinc 5 parts, and mercury. 



528 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

tendency among students to rely upon the rubber dam alone to 
prevent accidents. This is a fallacy, as the same results may occur 
with it as well as without it. The chief danger lies in the use of 
temporary stopping after placing paste. Capillarity and pressure 
often carry the paste to the cervical margin. Making the covering 
first or using fiber constitute the best precautions. 

In case of a very dangerous cavity, as a distocervical one, a special 
drill pit known as a " pocket " is to be made at some other point 
extending in the direction of the pulp horn and as near to it as can 
be made without too much infliction of pain. In this the arsenic is 
to be sealed while antiseptic sedatives are to be placed on cotton in 
the cavity of decay. This method is also valuable when the pulp is 
very irritable, and permits devitalization through a more or less 
healthy portion of pulp. 

The presence of pulp nodules may necessitate an application after 
lifting away the nodule (Fig. 404). 

The arsenical method may be used after a preliminary general 
anesthesia and bulb removal, or may even be used against an obdurate 
pulp canal filament. When pulp removal is intended the application 
may be removed through the opening and a probe may be passed 
into the pulp to test the progress of the devitalization. If needed, 
a second application may be made or the tooth may be temporarily 
closed. In case the pulp be found partially dead, it is better to 
allow more time for complete devitalization than to make a second 
application, as removing a portion relieves the congestion. 

Symptoms. — The large majority of pulps die under arsenic with 
but little pain. Sometimes throbbing pain results, passing into a 
heavy fulness as congestion supervenes. If too great, the pulp should 
be uncovered and bled slightly, then a sedative should be applied, 
iodin used as a counterirritant upon the gum, and pulp death awaited. 
Ordinarily the pain passes away as the pulp becomes more fully 
congested. Apical irritation may result and may be ignored if slight, 
or if severe be treated in the same way as the pulp irritation (Fig. 
412). A guard to prevent overocclusion is sometimes useful (Fig. 549). 

Accidents from Arsenical Applications. — If a portion of an arsenical 
application escape from beneath its covering, it may destroy much 
or a little gum tissue, according to the amount which escapes. The 
teeth should be seen early in doubtful cases and the condition of 
the gum observed. 

The arsenic may attack the gum festoon, inducing in it stasis 
followed by necrosis. The gum assumes a purplish turgidity, which 
later changes to a dirty yellow slough. 

The bone is usually devitalized for a distance. 



DEVITALIZATION OF THE PULP 529 

If the necrosis be self-limited, as is usually the case, a small 
sequestrum comes away after a few weeks. 

In some cases the arsenic may follow the festoon of the gum of 
one or more teeth, causing disagreeable sloughs and ulcerations. 
It may follow the pericemental tract, kill the pericementum, and the 
tooth drops out. In one case of a boy, aged twelve years, an appli- 
cation was made in a first lower molar. A blow from a base-ball 
was subsequently received and a slight leakage occurred merely a 
trifling slough of the gum being apparent mesially. Later the 
living gum margin appeared flabby and could be lifted away. Finally 
and gradually, during nine months, the buccal pocket deepened 
without loss of the gum, the tooth gradually loosened, the bone 
septum between the roots was found necrosed, the tooth was removed, 
and the socket healed without further necrosis. The alveolar process 
about one or several teeth may be devitalized and a sequestrum 
occur which includes the teeth. Certain toothache nostrums are 
sold which contain arsenic. Dr. G. C. Chance 1 records a case of 
arsenical necrosis occurring from this source. Dr. J. E. Powers 2 
records a case in which extensive necrosis occurred from the use 
of colored woolen yarn (as a cleanser of interdental spaces) which 
contained arsenic used in the dye. 

From the infirmary of the Philadelphia Dental College was re- 
ferred to the oral clinic a case of extensive coagulation necrosis, 
resulting from the rubbing of "toothache drops" upon the gum. 
Analysis showed the preparation used contained arsenic. Collapse 
from blood poisoning being the immediate danger, the child was 
operated upon by Prof. Boenning for drainage of the parts. During 
the recovery, the teeth from the right lower cuspid to the left lower 
second temporary molar, and the gums over the process, were lost, 
leaving a blackened alveolar process, to be later removed surgically 
(Fig. 454). 

Arsenic is liable to pass through the apical foramina of unformed 
or much resorbed roots. It may possibly pass through mature roots 
when an application is placed high up in the canal, rarely when applied 
under normal conditions (as recorded by some), or, as occurred in 
one case, by the application being pushed through the apex. It 
may be forced through in the act of broaching, or through the sub- 
sequent use of the cataphoric current or pressure anesthesia without 
the preliminary precaution of removing the arsenic. 

•In some cases arsenic has been applied to perforations made 
through the sides of roots under the impression that the vital tissue 

1 Proceedings of the Academy of Stomatology, Philadelphia, 1898. 

2 International Dental Journal, November, 1902. 
34 ' 



530 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

found was pulp tissue. In such case its necrotic effects will be noted 
upon the gum overlying the root apex or over the perforation, the 
tooth being loosened and extruded and may possibly be lost. 

E. C. Kirk 1 has recorded several cases of loss of teeth from arsenical 
necrosis of the pericemental tissue following the use of mummifying 
paste to pulp stumps previously impregnated with arsenic. His 
theory is that the arsenic was liberated by the affinity of the ingre- 
dients of the mummifying paste for the proteid constituents of the 
pulp tissue. The editor has often used such pastes after arsenic and 
without untoward results, and feels that some other element must 
have entered in Kirk's cases. 

Fig. 454 




Boenning's case of coagulation necrosis due to arsenic; shows exposed and blackened 

alveolar process. 



Such dangers as these demand that extreme precautions be taken 
against the careless use of quantities of the agent. The rules laid 
down should be adhered to. 

The only cure of the condition consists in the thorough removal of 
every particle of the arsenic. Any projecting masses of edematous 
gum should be cut away, as they are dead and will slough at any 
rate, and a freer access to deep parts is had — the blood-flow may 
itself wash away the arsenic. The forcible washing should be pro- 
longed and repeated, or 10 per cent, silver nitrate should be used to 
form arsenite. Dialyzed iron or tincture of iodin might be applied 
with a view to possible neutralization of the arsenic. 

The editor, in a case of known application of arsenic to an obscure 

1 Dental Cosmos, October, 1903. 






SPECIAL METHODS OF PREPARING PULPS FOR REMOVAL 531 

perforation, succeeded in causing regeneration of tissue by removing 
surgically the dead tissue and inviting repair. 

It may, therefore, be that after minute portions of arsenic, forced 
through foramina, exert their full effect, the resulting dead tissue 
may be removed by resorption or even exfoliation; indeed, this result 
has been noted in which no other explanation seemed possible. 

If the teeth are loosened and lost as the result of arsenical necrosis, 
either beginning at the gum margin or at the apical space, the alveolus 
will exhibit a bare periphery and even some odor of putrefaction may 
be present. The alveolus should be sterilized and the walls burred 
away to a tissue capable of healthy granulation. 

If suffusion occur, essential oils or phenol should be avoided in the 
subsequent treatment, as they tend to set the color by acting as a 
mordant (Kirk), rendering bleaching difficult. After the pulp is 
removed it is well to fill the apical portion of the canal, and then 
at once bleach with 25 per cent, ethereal pyrozone, after which 
the balance of the canal and the cavity may be filled. (See Moist 
Gangrene of the Pulp, p. 580.) 

Special Methods of Preparing Pulps for Removal. — A fully exposed 
pulp in a single-rooted tooth or single root of a multirooted tooth, 
may be suddenly "knocked out" by means of a delicately pointed 
orange-wood stick or Portuguese toothpick. The point is dipped in 
carbolic acid and suddenly and boldly driven into the pulp, either by 
hand or mallet force. The method is not so agreeably delicate as 
pressure anesthesia, but is effective. It must not be used in partial 
exposure, as, not reaching the apex, it may cause pain. Its use is 
only indicated in emergency or occasionally in crown work after 
excision of the crown by excising forceps. 

A vital remnant of pulp may be removed after instilling a strong 
cocain solution, or carbolic acid, or a paste of carbolic acid and 
acetate of morphin, into its substance by means of a "puncture 
probe." This instrument may be made by filing down a Donaldson 
bristle to a fine point, which is further whetted on an oil stone. The 
sides of the probe are polished by folding a cuttle-fish disk upon 
itself, holding it between the thumb and forefinger of the left hand, 
and drawing the probe through it. The pulp canal is flooded with 
the carbolic acid, and gentle thrusts are made into the pulp until the 
probe is stopped at the apex. If it pass through, that must be judged 
by the sense of touch. Custer recommends 75 to 90 per cent, sul- 
phuric acid as superior to carbolic acid. At times a small end of 
pulp filament may be seared with a hot Evans' root drier, which is 
quickly thrust into it. This does not necessarily give much pain. 

A slow but effective method of disposing of these filaments, when 



532 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

hyperirritable or when patients are timid, consists in packing a 
cotton twist saturated with carbolic acid containing cocain hydro- 
chlorate in solution into contact with the pulp, and then gently 
compressing the pulp. The cotton is to be left in position for a day 
or two, when, as a rule, the pulp may be removed. It induces throm- 
bosis, and carbolic acid may be used with pressure to produce 
anesthesia at the time of operation. A dressing of tincture of iodin 
has been suggested for the purpose. 

Devitalization of Pulps in Temporary Teeth. — All of the anesthetic 
measures are as applicable to temporary teeth as to the permanent 
ones if the little patient will tolerate their application. 

If the child present an exposed pulp in a tooth the roots of which 
are not resorbed, arsenic much diluted, may be applied for twenty- 
four hours and then be removed, the pulp being then allowed to die. 
When roots are resorbed it is better to cap the pulp with Jodo- 
Formagen cement, or if necessary, apply a pellet of cotton wet with 
phenol, then touched to iodoform, and seal in with temporary 
stopping, making a slight pressure. This may remain a week or 
more and be renewed if necessary. 

Darby has used cantharides, -j-q grain in carbolic acid, with success. 
It must be carefully sealed, as strangury is a possibility. 1 Figs. 146 
and 116 are guides as to the condition of the end of the root. 

THE EXTIRPATION OF THE PULP. 

After the pulp is prepared for removal or the patient is anesthe- 
tized, free access to all parts of the pulp cavity and canals must be 
obtained. This is usually best accomplished by an opening made in 
direct line with the axis of the pulp canal. In general terms this 
involves for sound teeth an opening upon the lingual surface of 
incisors and cuspids and upon the occlusal surface of bicuspids and 
molars. 

This access may consist of a new opening or an extension of a 
cavity, or at times the cavity and canal may simply be made con- 
tinuous. 

When a cavity of decay exists the pulpal wall should be perforated 
and a large bud bur should be used to cut away the dentin over- 
hanging the pulp cavity. It is usually necessary to extend the cavity 
in the central occlusal direction, so as to permit direct access to 
each canal (Figs. 455 to 462). 

When a tooth crown would be irremediably weakened by such a 

1 Dr. J. Foster Flagg had such a case. 



THE EXTIRPATION OF THE PULP 



533 



course, a slight indirectness is permissible when flexible cleansers 
can be used instead of drills. This leaving of tooth structure should 
be done with judgment. The canals must be cleansed. In cavity 
approaches the ouier wall of the pulp cavity should be cut away to 
permit an obtuse-angled approach rather than a right-angled one 
(Figs. 460 and 462, A). All pulp cavity corners should be burred to 
a shape that obviates retention of pulp debris, the subsequent decom- 
position of which would lead to discoloration. The opening shown 
in Fig. 458 is faulty for this reason, and is better if extended more 
toward the incisal edge, making an oblong opening with rounded 
ends. 



Fig. 455 




Fig. 457 



Fig. 458 






Fig. 459 



Fig. 460 



Fig. 461 



Fig. 462 







In sound teeth the entrance to the canal is made with a small 
spear drill, after the enamel has had a "spot" made in its surface 
with a sharp dentate bur. This centres the spear drill and prevents 
its slipping about. After it has entered the pulp cavity dentate burs 
are used to enlarge the opening to the desired' size and shape. A 
sawing motion creates more rapid clearance and cutting of tooth 
tissue. 

One should not always suppose that the spear drill will drop into 
an appreciable pulp cavity. The careless driving of a drill into a 



534 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

tooth may cause a perforation. Secondary dentin or a large nodule, 
and, in previously treated teeth, zinc phosphate may occupy the 
pulp chamber. Therefore, when doubt arises, open well that portion 
of tooth or filling which has been drilled through, and note the 
conditions, then go ahead carefully. In opening a located pulp 
chamber with burs a bud bur is very useful, but all burs once placed 
through the drill hole and into the pulp chamber must be used 
laterally or the heel of the bur used with an outward sweep toward 
the occlusal aspect for the sake of safety. 

Fig. 463 



Kerr or Downie broaches. Various finer sizes of these broaches and reamers may- 
be had. They should have accurate taper. 



The canal (or canals) is now to be explored, and if of operable 
size a Donaldson cleanser or barbed broach is passed to the canal 
apex, twisted so as to engage its teeth with the pulp substance, 
and the pulp extirpated. 

If there be any difficulty in finding the canals after this preparation, 
by reason of the broach catching on the edge of the orifice, the mouth 
of the canal should be made continuous with the wall of the pulp 
chamber by means of a small bud bur. The wall then leads the 
broach into the root lumen. 

In single-rooted teeth with finer apices a fine Kerr engine root 
reamer (Fig. 463) may be passed by hand to the apical portion of 
the root and gently rotated. It is then mounted in the hand piece, 
passed gently to the apex, slightly withdrawn, and then operated by 



THE EXTIRPATION OF THE PULP 



535 



engine power. It is pressed lightly laterally to enlarge the canal 
slightly. The next larger size is then used in like manner, and 
finally the larger admissible sizes. This gives a beautifully tapered 
canal form useful in canal filling and for the adaptation of dowels. 
The pulp is simultaneously removed, generally being churned out 



Fig. 464 



Fig. 465 



Fig. 466 



Fig. 467 



Fig. 468 



i 



Donaldson's pulp-canal cleansers. 



IJ 



of the root, and danger of false openings is 
avoided. A final exploration and apical 
scraping may be given with a fine Don- 
aldson cleanser (Figs. 464 to 466), and 
the pulp cavity corners rounded out with 
burs. ' 

This technique is only admissible in cases 
of openings in line with the pulp axis. 
Those almost in such line may have the 
flexible sizes of Kerr reamers so used, all 
apexward pressing and reaming to be done 
by hand at first. When general anesthesia 
is employed it is better to open roughly, 
then pass a fine Donaldson cleanser, which 
has been previously dipped in carbolic acid 
and laid aside in readiness, to the apex of 
the root canal. It is given a few turns to 

engage the pulp, and the latter is lifted away. The other work is 
to be done upon return to consciousness. 

As the Kerr broaches and reamers are made of a variety of forms, 
it should be stated that only those which have a gradual taper from 
point to shank can be relied upon to satisfactorily carry out this 



Donaldson's spring-tem- 
pered nerve bristles. 



536 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

technique. In these the successive sizes follow one another without 
danger of perforation of the canal walls. 

It is sometimes better to drive a fine hand Kerr broach to the canal 
apex, and, if the engine broach be not permissible, to continue with 
the different sizes of hand broaches. One soon obtains a familiarity 
with the canal curve and size when working with the hand which 
gives confidence and safety when later working with engine power. 

In molar teeth and upper first bicuspids, after the pulp chamber 
has been prepared, the canals are to be located with a fine smooth 
broach or a Kerr broach. The finest root reamer is then used by 
hand and gently twisted and forced apexward into each canal in 
turn. The next smaller is then used. As these canals are normally 
somewhat curved, only flexible forms should be used unless the 
larger size follows readily the rather curved canal made by the 
previous one. Following this, Donaldson cleansers are operated by 
hand to scrape the sides and inequalities of the somewhat flattened 
canals which the reamers have not reached. 

In place of drills the process of canal enlargement devised by 
Callahan 1 may be employed. The general cavity wall is varnished 
to prevent the action of the acid upon the dentin, and by means of a 
pair of Flagg's dressing pliers or a minim dropper a drop of sul- 
phuric acid (50 per cent, solution) is deposited at the mouth of the 
canal to be operated upon. The finest size of Donalson's canal 
cleanser is then passed into the canal as far as it will go, using a 
pumping movement to carry the acid farther into the canal and to 
scrape the canal walls softened by the action of the acid. The acid 
chemically destroys any organic matter — i. e., pulp tissue — present, 
releases the calcium of the dentin from its combination, and forms 
calcium sulphate, which is mechanically removed by scrapers. Care 
must be observed not to strain the broaches too greatly, as they may 
break. The operation is continued until the apex of the root is 
reached. F. T. Hayes suggests the use of aqua regia as less injurious 
to broaches; lactic acid is also less injurious. When the cleanser will 
not enter readily it is well to file away the barbs from an old cleanser 
and leave it roughened, and to use it for a time with the acid until 
the cleanser proper can be employed. Even then it may be necessary 
to use a cleanser with only part of the barbs filed away. Iridio- 
platinum or gold broaches may be used for this purpose. 

Some operators prefer the use of the alloy kalium-natrium, used 
on the broach as a means of facilitating the opening of the canals. 

In the canals of posterior teeth short cleansers are mounted in a 

1 Proceedings of the Ohio State Dental Society, 1894. 



THE EXTIRPATION OF THE PULP 



537 



chuck handle and the shank sharply bent at a right or obtuse angle. 
If the cleanser bind in the canal, it should be grasped with the thumb 
and forefinger and given a straight pull to relieve it. 



Fig. 469 



Fig. 470 





Fig. 471 



Fig. 472 





If acid be used it should be neutralized with sodium bicarbonate 
or sodium dioxid. The improved Gates-Glidden drill (Fig. 473) 
has some use in the enlargement of canals the lumen of which has 
been determined by the above methods. They should not be used 
for the preliminary opening of fine canals, as they tend to form 
false channels in the side of the canals which constantly catch even 
fine bristles and may render a canal into a form even less advan- 
tageous than that it already possesses. The canal filament of pulps 
in molars and upper first bicuspids may be lifted away with barbed 



538 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

broaches or cleansers if the canals are large, but it is ordinarily 
a waste of time to attempt it in the finer canals, as the other work 
must be done in the apical regions. 

The use of 5 per cent, formalin, tannin, or alum, to be specially 
applied about two days after the application of arsenic, has been 
suggested for the toughening of pulps. Their use necessitates a visit 
for their special application. They toughen the pulp, and, while 
the advantage in pulp removal is offset by the special visit needed, 
may, in fine canals, mummify inaccessible portions of pulp tissue. 

The point of importance is the removal 
Fig. 473 from the pulp canal of all removable 

portions of pulp tissue and an enlarge- 
ment sufficient to admit a satisfactory 
root filling. It is an open question 
whether in multirooted teeth this is ever 
complete, or whether it is necessary that 
it be made absolutely so, regardless of 
ner^canaf dr^T^or^nglne other dangers. In molars and even other 
work. teeth there may be more than one for- 

amen and at times delta-like formations 
are present. Therefore one should use all safe means and rely upon 
antiseptic measures for the impossible cases. In this connection a 
radiograph before and after canal exploration will be of assistance. 
A perfectly safe rule for mechanical procedures is as follows: Use 
drills only when they advance readily into the root lumen; prefer 
Downie broaches and Donaldson cleansers under other circum- 
stances. Advance no large reamers into delicate apical portions of 
roots, as a lateral perforation may be made. If a fine broach cannot 
be passed through the apical foramen, do not attempt its enlarge- 
ment; and it is better to preserve a normal foramen, as large for- 
amina present greater difficulty of filling than normal ones. 

If doubt exist as to the presence of a portion of pulp in the apex 
of the root, papain paste may be placed in the canals for a few days 
to digest the remaining pulp tissue. (See Pulp Digestion.) 

If the pulp be removed as far as possible by careful work and the 
canal sealed to that point with a mechanically perfect and anti- 
septic root filling, it is improbable that any future trouble will arise, 
and it is better that any such trouble should be subsequently treated than 
that immediate trouble should be set up by perforation in an endeavor 
to force a finding of canals which a very fine Downie or Kerr cleanser, 
or broach, will not explore. 

This technique is, as a rule, best carried out under rubber dam, to 
prevent the septic contamination of canals by entrance of infected 



THE EXTIRPATION OF THE PULP 539 

saliva; but if this be impossible it is wise to sterilize the mouth and 
napkin it, and to place a drop of carbolic acid or formocresol in the 
canals and continue the work under antiseptic precautions. 

It is wise to have the patient first brush the teeth, using soap or a 
tooth paste or powder. After application of the dam or napkin the 
cavity is cleansed of the debris of decay if any be present. Then 
the cavity is to be wiped out with phenol camphor. Next the appli- 
cation of cocain, etc., is made. Before entering the pulp chamber 
or just after, a drop of formocresol is to be placed on the field of 
operation and a clean bur used to enter the pulp cavity. The debris 
is removed, the canals located, and a fresh drop of formocresol 
placed before continuing with the canal work. 

As the napkins become wet they may be removed, the cavity 
douched with a jet of warm water, the patient rested for a moment, 
and then the napkins are reapplied, the cavity dried, and the opera- 
tion repeated. The napkins may be renewed without disturbing the 
treatment, but it is often desirable to wash out the debris, and 
the rest is often agreeable to the patient. 

The scraping of the canals removes the possible remnants of 
pulp tissue, odontoblasts, etc., adhering to the dentin walls, and 
also a part of the wall with the large ends of the fibrils. All these 
are decomposable media, may become septic, and are wisely removed. 

The final removal of all pulp debris, coagulated blood, etc., is best 
done with a fine Donaldson cleanser, moved to and fro in the canal 
with one hand, while with the other a stream of warm water is gently 
introduced by means of a Moffat syringe. A large cottonoid roll 
or a napkin may be held by the patient or assistant to absorb the 
excess of moisture when the rubber dam is in position. 

If the operations have been done under antiseptic precautions, 
the root is ready for filling, unless irritation of the apical tissues be 
severe, in which case a sedative antiseptic — e. g., menthol in chloro- 
form — on cotton should be sealed in the canal. The gum should be 
painted with iodin as a counterirritant, and the subsidence of the 
symptoms awaited. (See Non-septic Apical Pericementitis.) 

Rhein recommends for the treatment of inaccessible portions of 
recently devitalized pulps the use of a chemically pure zinc point, 
to be placed in the root moistened with a 1 to 500 mercuric chlorid 
in hydrogen dioxid (3 per cent, solution) and the anode of the cata- 
phoric appliance applied to it, the cathode sponge to be placed under 
the dam on the cheek. From 1 to 5 milliamperes of current are 
used and maintained for from three to seven minutes, according to 
the exigency. 

Zinc oxychlorid is produced and carried into the tissue. 



540 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

It is always, perhaps, safer to introduce a sealed dressing of phenol 
camphor plus menthol or thymol until all possible hemorrhage or 
irritation has subsided. In case of pressure anesthesia with free 
hemorrhage a little alum and thymol, equal parts, is well added to 
the phenol camphor, or even a dry dressing, to absorb any secondary 
hemorrhage. (Ottolengui.) 



DESCRIPTION OF FIGS. 474, 475, AND 476.' 

Fig. 474. — Fig. 3 gives in contrast a sectional view of deciduous and permanent upper 
teeth divided through their lateral diameters. 

Fig. 4, a sectional view of the corresponding lower teeth divided through their 
anteroposterior diameters: a, b, c represent respectively the deciduous and permanent 
front incisors in contrast; d, e, f, the lateral incisors; g, h, i, the canines; k, deciduous 
molars, upper and lower; I, m, the successors to the deciduous molars, the bicuspids; 
n, o, represent permanent molars; c, /, i, m, o, have dotted lines indicating the thickness 
of enamel removed by wear, atrophy of the cementum, and reduction in the size of the 
pulp due to progressive calcification, these changes being incident to old age. 

Fig. 475 erpresents in Fig. 1, letters a to h and a to h, the longitudinal or vertical 
sections of the sixteen upper teeth, showing the labiopalatal diameter of the pulp 
chamber and canal in crown and roots, the section of the molars being through the 
anterior buccal and palatal roots, while the bicuspids d e and d_e illustrate the result 
of such a compression of the root as to divide the pulp chamber into two canals — a 
condition which so frequently exists in these flattened roots. The double-lettered 
series, d d to h h and dd to hh, represent in the molars a section through the posterior 
buccal and the palatal roots, from which is quite readily recognized the slightly greater 
lateral diameter of the pulp chamber in the crown and the larger canal in the posterior 
buccal root over that in the anterior buccal root, while the bicuspids lettered eedd 
and dd e e illustrate modified pulp chamber and canal, with bifurcation of the root 
in one, these being cut through a different axis or plane from the single-lettered series. 

Fig. 2, letters a to h and a to h, represent the sixteen lower teeth with the section 
through their long diameters, as in the upper series. These incisors illustrate the 
compressed or flattened condition of their roots in contrast with the cylindrical char- 
acter of the roots of the upper incisors, while the bicuspids d e and de illustrate the 
singleness of their pulp chamber and the cylindrical condition of their roots as in 
contrast with the flattened or compressed condition of the roots of the upper bicuspids. 
The molars /, g, h, and /, g, h represent sections through the anterior root, illustrating 
its compressed condition and divided pulp chamber in the first and second molar, 
and a somewhat flattened one in the anterior root of the third molar; ff,gg, hh and 
f f, g g,hh represent the single and cylindrical pulp chamber in the posterior root of 
the lower molars, while b b f c c and a a, bb represent the incisors and canines of the 
same series, with modified pulp chambers arising from modified development. 

Fig. 476. — Fig. 1, from a to h and a to h, represent the upper teeth, with transverse 
or horizontal section through the base of the pulp chamber in the crown, viewing 
the entrance to the canals of the several roots, while the same letters in Fig. 2 represent 
the lower series in the same manner. 

Fig. 3 represents the upper teeth, with the transverse or horizontal section made 
below the largest diameter of the pulp chamber and through the canals after they 
have diverged from the central chamber, but before the roots into which they run have 
in the molars bifurcated. 

Fig. 4 in like manner represents the lower series, well illustrating the flattened or 
compressed condition of the canal anterior roots of the molars and the division of the 
chamber, as is frequently found in the roots of the lower incisors. 

The letters a a,bb, c c, dd, f f, d d, and e_e (Fig. 3) represent the relative shapes, 
whether circular, oval, or flattened, of the pulp canal in the roots of the upper central 
and lateral incisors, the canines, the first and second bicuspids, and the first, second, 
and third molars, while the same letters in Fig. 4 represent the relative shapes of the 
pulp canal in similar teeth in the lower series. 

1 These figures are taken from v. Carabelli 's Anatomie des Mundes. 




ib<- 






THE EXTIRPATION OF THE PULP 



543 



A 













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fcb 



if 



' ^ti f) 




CX 



3j 



/ 




*>/> 










to 







^ 

^i 
% 



ft * 



// 




%. 



66 




V * 





y 



^ 

a 








&b 







€3 




3) 



$M)^ 



/ 



544 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

Sometimes it is desirable to mummify any possible irremovable 
portion of pulp or the fibrils by the use of formalin solutions which 
are usually tolerated. 



Distal 




Fig. 478 Fig. 479 Fig. 480 



mesial 



Diagram illustrating the improvement in ac- 
cess C, to the deeper portions of enamel by cut- 
ting in accordance with a radiograph. The 
dotted line shows the ordinary opening per- 
mitting the access b b. (Rhein.) 




Upper lateral incisors. (Otto- 
lengui) . 



Fig. 481 



Fig. 482 



Fig. 483 




Fig. 484 





Upper canines. 
Fig. 485 




Fig. 486 




Upper first bicuspids. 



The carrying out of canal treatment involves a knowledge of the 
topographical anatomy of the teeth and their pulp canals. As an 
aid to this Figs. 474, 475, and 476 are introduced, showing the normal 



77//: EXTIRPATION OF THE PULP 



545 



outlines of the teeth and their pulp chambers; Fig. 476 shows the 
appearance and locations of the pulp canal openings at their coronal 
ends. It is to be borne in mind that the roots are not always normal 
as shown in Fig. 475, and that various degrees of lack of development 
or resorption may cause the root canals to be unusually open or short, 
with the treatment complicated by the presence of vital tissue at the 
root ends. In a general way it may be stated that much resorbed 
roots, as indicated by the age in deciduous teeth, or largely incom- 
plete roots, as indicated by the age in permanent teeth, indicate 
a pulp-capping operation rather than extirpation; in the permanent 
teeth, to permit better root formation. If unavoidable, one must 
do the best possible. 



Fig. 487 



Fig. 488 





b a 

Upper second bicuspid. 



b . a 

Upper first molar. 



Fig. 489 



Fig. 490 



Fig. 491 






Upper molar. 



b a 

Upper second molars. 



In the penetration and enlargement of canals the larger and 
straighter canals may be cleansed thoroughly to the apex, but in 
very fine and tortuous roots (Figs. 478 to 507) the operator is often 
confronted with the option of taking the chances of perforation 
by forcing further entrance or of leaving some doubtful apical 
portion uncleansed. To further perfect the operation of canal cleans- 
ing a radiograph may be taken as indicated by Rhein, and the 
cavity extension made so as to permit as direct an access as possible 
(Fig. 477). In very bad cases the decision should be that the danger 
35 » 



546 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

of perforation is the greater evil, and agents of a mummifying 
character should be employed to render any such filament into a 
state lessening the danger of subsequent putrefaction. 



Fig. 492 



Fig. 493 



Fig. 494 






Fig. 495 



Fig. 496 



Fig. 497 






Upper molars. (Ottolengui.) 



Fig. 498 



Fig. 499 





Upper third molars. 



The writer regards the use of formocresol (equal parts of 37 per 
cent, aqueous formaldehyd solution and cresol) as especially valu- 
able where immediate root filling is not indicated. If the patient be 
of a nervous and irritable type this may be diluted to 5 or 10 per cent, 
formaldehyd strength by the use of cresol or camphophenique with- 
out impairing its value. Often the full strength may be used on 
cotton as a temporary dressing. This hardens any remaining pulp 
and also probably the fibrils in the tubules. It also permits the 
apical tissue to heal and resume its normal sensitivity when the 
pulp has been entirely removed, which is of value in determining 
the extent to which pressure may be applied in filling the canals. 
In anterior teeth it is better to use aqueous formaldehyd solutions, 
as the cresol may cause discoloration, but in these situations more 
perfect mechanical work can be done. 



THE EXTIRPATION OF THE PULP 



547 



In a few cases in which cervical cavities obliterate the canal or 
cause annoying approach to it, it is desirable to remedy the con- 



Fig. 500 




Fig. 504 





Fig. 501 




Lower bicuspids. 



Lower first molars. 



Fig. 502 





Fig. 505 





Lower first molar. 

Fig. 506 



© 




Lower second molar. 



Lower first molar, immature. 
Fig. 507 




Lower third molar. 



dition. In such case the canals are opened as usual and enlarged, 
and the cavity prepared with suitable retentions for filling. The 
last-used reamer is then to be placed in the canal and the filling 




548 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

inserted. The filling is then supported by pressure while the reamer 
is slowly twisted to the right and withdrawn, leaving a canal through 
the filling. This may be done with amalgam or with zinc phosphate 

if a later removal be required. If the 
Fig. 508 root be much weakened, a tapering dowel 

may be cemented through the crown 
and canal, thus attaching the root to the 
crown more firmly (Fig. 508, also p. 432). 

ACCIDENTS IN CANAL OPENING. 

The chief accidents that may occur are 
the perforation of the root wall and the 
breaking of the instruments used. If the 
technique laid down be carefully followed 
Method of restoring lost the danger of perforation is practically 

canal continuity. The cavity v • j. j t i? j. xi_ xxj 

should have more retention eliminated. In fact, the greatest danger 
form than shown: a, amalgam, is the penetration and enlargement of the 

apical foramen. To avoid this the Kerr 
reamers should always be passed to the apex of the canal by hand 
or while the reamer is not revolving. It is then withdrawn a trifle and 
revolved, and one may always judge the distance the reamer was 
withdrawn. Accidents are usually the result of thoughtless forward 
pressure of reamers and drills, and care will reduce this to a minimum. 
Sometimes one must take the chances with the Kerr engine reamer. 
When doubt exists as to canal locations, the desiccation of the 
pulp chamber is of great assistance by bringing them into view, and 
if secondary deposits exist one should always use a small bud bur 
and keep well within the limits of the dentin of a root while gently 
seeking a canal lumen. 

Frequent exploration should follow gentle advances, and, as a 
rule, the canal will be found of fairly normal size just beyond the 
point of constriction. In some cases 50 per cent, sulphuric acid 
should be sealed against the suspected canal and the operation 
deferred to another sitting. 

If a perforation be accidentally made it should be covered as in 
any case of perforation (which see) . 

Always one should be able to diagnosticate such an opening and 
arsenic should never be applied to such. Cases of extensive necrosis 
have occurred from carelessness in this direction. The breakage of 
broaches is largely avoidable through the use of new instruments and 
by adhering to the rule of using the smaller sizes until the canals are 
sufficiently enlarged to permit the use of larger sizes, and, in case of 



ACCIDENTS IN CANAL OPENING 



549 



engine 
canal. 



509 



I 

1 



reamers, of starting the power with the reamer loose in the 
The engine broach seems to be of better temper than the 
engine reamer. 

Accidents of this sort usually occur with barbed instruments of 
the Donaldson cleanser type, especially when used with force. 
Sulphuric acid tends to disintegrate the 
broach, so that lactic acid is often better 
used with it, or the alloy of sodium and 
potassium with a smooth broach will open 
the canal so that the cleanser will not bind. 
If it does it should be grasped with the 
thumb and finger and given a straight pull. 

While avoidance is far better than the ap- 
plication of the remedy, if the accident occur, 
the broach should be removed if possible. 

If lying loosely in the canal a new cleanser 
may be passed to one side of it and then be 
pressed against it. It should engage the 
barbs and jig it out. 

Cotton wrapped on a small Swiss broach 
may be pressed down at one side of the 
broken broach and its fibres made to engage 
its barbs. 

Moving the broach back and forth while 
sulphuric acid, sodium dioxid, or sodium and 
potassium is about it, will sometimes loosen 
it. One' may sometimes drill to one side of a 
broken instrument with a Kerr hand broach 
in order to more readily engage it with a 
barbed instrument. If very loose a magne- 
tized probe will attract it and draw it out. 

If the broach be tightly fixed in the canal, 
sodium chlorid, tincture of iodin, sulphuric 
acid, aqua regia, or 25 per cent, pyrozone 
may be sealed in, in the hope of chemically 
disintegrating it. 

The head of a Gates-Glidden drill or Kerr 
reamer is treated in the same manner. Some- 
times in straight roots the How appliance shown in Fig. 509 is useful. 
If* any broach be irremovable, iodoform paste or embalming paste 
should be packed over it and sealed in, in order to keep the part 
permanently sterile. In a septic case the formocresol treatment 
should precede such root filling. 



Split and threaded in- 
strument for engaging 
the shank of a Gates- 
Glidden drill. 



550 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

THE FILLING OF ROOT CANALS. 

In all cases in which the removal of the dental pulp from the 
canals is necessary, it is imperative that the pulp canals shall be 
filled with some substance that shall mechanically obliterate it 
by sealing it throughout its length, in order to prevent the ingress 
of fluid either from the mouth or apical tissue. Such fluid is liable 
to putrefaction, and the results of putrefaction follow. If made 
antiseptic, it also tends to kill out any bacteria which may find 
a partial entrance. The mechanical sealing may be defective, even 
when the best possible effort is put forth to make it perfect, so that 
the addition of more or less permanent antiseptics is valuable. 
Prinz has suggested that it should be impervious to x-rays so that 
it may be radiographed. 

It matters little whether a canal filling is hard or soft provided it 
seals the canal permanently, that it is permanently antiseptic, non- 
irritating, and that it is not disturbed by any subsequent work. It 
is better that it be capable of removal with a reasonable amount of 
safe work. 

It also makes very little difference whether the pulp has been 
removed while aseptic or has been in a septic state, provided the 
canal has been rendered sterile by appropriate means. 

In other words, when the canal is aseptic and the apical tissues 
sterile and healthy, the canal is ready for filling. The length of time 
this may require also makes no difference. Therefore, what is here 
said applies to all cases requiring root filling. Much has been written 
of the impossibility of sterilizing the tubules of root canals and of 
the liability of return of sepsis from bacteria located in them. This 
simply means that one should employ the best means of gaining 
sterility known and then employ permanent antiseptics. To seal 
and keep these tubules as sterile as possible, the use of a thin varnish 
of resin, 12 grs., in chloroform, f5iij> has been suggested by Callahan 
to be applied after desiccation and before root filling. The size of 
the apical foramen, the presence of inaccessible apical portions of 
canals, the presence of perforations and some other conditions, 
however, indicate a choice of some root filling rather than others, 
so that there is no absolute rule for all cases. 

The following root canal fillings are useful. 

Gutta-percha.— This is usually the ordinary, low heat, pink gutta- 
percha base plate containing vermilion and zinc oxid. Cones may 
be rolled or left with flat sides. Prepared cones may be purchased 
which have an accurate taper and are either round or flat-sided. 
The flat side permits any adjunct plastic filling material or solvent 



THE FILLING OF ROOT CANALS 551 

to flow down the side of the cone rather than be forced toward the 
apex. 

Temporary stopping may be melted in a spoon and aristol added 
to it. It is then rolled into cones for use. Instead, a stick of it may 
be warmed at a point away from the end and then be pulled out into 
two cones which may be further rolled out. They may be rolled in 
powdered aristol if desired. 

Ottolengui advises the use of bits of floss silk an inch long to be 
saturated with chloro-percha and dried. These are to be pressed 
into chloro-percha previously placed in the canal and crimped to 
place. An end is left projecting into the pulp chamber. If necessary 
this may be caught and the dressing withdrawn. 

Chloro-percha. — This is a solution of gutta-percha base-plate in 
chloroform. Usually a quantity of aristol or iodoform is added to 
make it antiseptic. As it shrinks in hardening it should be used in 
conjunction with gutta-percha cones or carried upon cotton twist 
or upon floss silk, which it saturates, transforming them practically 
into a solid mass when the chloroform evaporates. 

Euca-percha.— The basis of this substance is a solution of gutta- 
percha base-plate in eucalyptol. To this various antiseptics may 
be added. There are various modes of making this substance. 
B. L. Cochran 1 suggests the following: 

1$ — Gutta-percha base-plate gss 

Dissolve in chloroform q. s. to a thin solution. Jfcy - 

Add saturated solution of thymol in eucalyptol . . . fgss 

Let the chloroform evaporate. 

Euca-percha Compound (Buckley, Lilly) is a simple solution of 
base-plate in eucalyptol made by aid of heat. 

Formo-percha (Blair) has paraform and oil of cassia added. 

This material may be warmed into a creamy paste and be used 
either on cotton or be used in conjunction with gutta-percha 
cones. 

Zinc Oxychlorid. — This consists of the ordinary zinc oxychlorid 
cement, which consists of modified calcined zinc oxid for the powder 
and diluted zinc chlorid as the fluid. 

It is antiseptic for a time at least, and may have iodoform incor- 
porated with it if desired. It is carried to place on a thread of cotton, 
or may be used with gutta-percha cones. The addition of a trifle 
of« glycerin retards setting. 

Embalming Paste. — A so-called embalming paste is prepared as 
follows : 

Dental Review, 1905. 



552 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 



Or, 



1$ — Paraform 1 part 

Thymol 1 part 

Glycerin 1 part 

Zinc oxid 1 part or more. 

1$ — Paraform 1 part 

Thymol 2 parts 

Alum 1 part 

Zinc oxid 2 parts 

Creosote to a thick or thin paste. 



This is used as a temporary germicidal canal dressing on cotton 
or as a root-filling with gutta-percha or temporary stopping cones 
which are pressed into it, 



Fig. 510 



Fig. 511 





Radiograph of a perfect gutta-percha root 
filling. (Rhein.) 



Root-canal filling: A, gutta-percha; 
B, zinc oxychlorid. 



Wax or Paraffin. — Either of these may have a third of its bulk of 
salol, aristol, or iodoform, or a fifth of paraform added to it while 
melted in a spoon. It is then rolled into cones or small pellets. In 
use a pellet is dropped into the dried pulp chamber and a hot Evans 
root drier point applied. As it melts, the metal point is carried down 
into the root and the fluid material pumped to the apex. Capillarity 
does part of the work. It adjusts itself to the tissue and the canal 
walls. The pulp chamber is then cleared of excess wax, etc., and 
filled without pressure. 

Prinz 1 recommends the use of hard paraffin having a melting 
point of not less than 132° F. in the following combination: 

1$ — Thymol 2 parts 

Bismuth trioxid 30 parts 

Hard paraffin 68 parts 



The canal is to be thoroughly dried, then merely moistened with 
liquid albolene, a cone of the compound then to be placed in the 

1 Dental Cosmos, October, 1912, p. 1089. 



THE FILLING OF ROOT CANALS 



553 



canal ami melted with a root drier (an electric drier or Evans' or 
Reithmuller's modification 1 ). The albolene combines with it and 
leads it to place with exclusion of air. The bismuth is added to 
make it impervious to the .T-rays, hence it throws a radiographic 
shadow. 

Prinz states that iodoform added to paraffin can be only super- 
ficially antiseptic. This is, however, quite sufficient. Mixed into 
wax it persistently odorizes the air in its vicinity, hence should 
have antiseptic value. The influence of iodiform for long continued 
usefulness is unquestionable. 

Salol. — This is a solid antiseptic, melting at 104° F. It is used 
much as paraffin is. A gutta-percha cone may be thrust into it 
while fluid. It often seems to disappear from canals, and unless 
used with paraffin is to be used only as a temporary root filling. 



Fig. 512 



Fig. 513 




A, perforation through side of apex; 
D, cone of gutta-percha passing through; 
B, portion to be cut off; C, portion of 

canal not treated. 




Lateral perforation due to holding a 
bur at a wrong angle to the axis of the 
root: A, root canal subsequently filled 
with gutta-percha; B, perforation filled 
with a fitted cone of gutta-percha; C, 
zinc oxy-chlorid. 



Canada Balsam. — A solution of Canada balsam in chloroform to 
which hydronaphthol is added (Williams) makes a useful solution 
in which to saturate cotton twists or to moisten canals previous to 
the introduction of a cone of gutta-percha. Balsam of Peru is now 
on trial, but its soft condition is liable to render it a failure. 

Colophony. — Callahan 2 recommends violin resin, grain 12, in chloro- 
form, 3 fluidrams, as a thin solution for filling the desiccated tubuli. 
The canals having been reamed to permit cones to enter, they are 
filled with the solution and a gutta-percha cone pumped back and. 
forth forty to sixty times to dissolve the cone and force adaptation. 
The cone is then packed in with pluggers touched to a cake of 
paraffin. 

1 See Dental Cosmos, March, 1913, p. 342. 

2 Journal of the Allied Sciences, March, 1914. 



554 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

Normal Tapering Well-opened Canals. — In these canals gutta-percha 
is admirable; a little eucalyptol is applied to the canal walls and a 
section of a suitable cone mounted by heat on the end of a canal 
plugger which will go to or nearly to the canal end is gently but 
firmly pressed into the apex of the canal. Temporary stopping cones 
are more readily adapted, and as they can be made antiseptic, are 
valuable. 

The rest of the canal is then filled with other sections or with zinc 
oxychlorid made thin and carried to place on cotton twists. The 
latter may be used for the entire canal, and should then be preceded 
by a tiny bit of cotton saturated with an essential oil to prevent 
irritation of the apical tissue. It is claimed that this cotton is acted 
upon by the zinc chlorid, being transformed into an amyloid condition. 
If used alone a slight degree of moisture aids in carrying to the 
apical foramen (Fig. 513). 

A variant consists in moistening the canal with chloro-percha or 
euca-percha, and using the section of cone or pressing in an entire 
cone. A second cone may be placed at the side of the first and 
both compacted after warming with a hot air blast, or the first cone 
alone used. 

Another variant is the use of chloro-percha on cotton, which makes 
a very accurate and easily introduced root filling when carried to 
place on a properly formed and tempered Swiss broach or prepared 
Donaldson bristle. A little iodoform may be taken up with it. 

When the broach must be bent to enter canals, loosen the broach 
first before introducing into the canal, thus leaving the cotton 
loosely mounted on the broach. To prepare a Donaldson bristle cut 
off the hook and flatten the end upon an Arkansas stone, and slightly 
flatten on two sides, then lay upon a glass slab and burnish thor- 
oughly to remove any bur left. In use the cotton and broach are 
rolled with the left forefinger and thumb only. It is obvious that 
to do this the broach must be perfectly straight. When slightly 
bent the method of rolling the cotton next described may be em- 
ployed. The writer believes the prepared Swiss broach not only 
more facile but economical in use. 

To prepare broaches, select accurately tapering Swiss or English 
broaches from which the temper has not been drawn. Next, draw 
the temper by placing a few in a test-tube and heating first at the 
shank, gradually drawing the tube over the flame toward the points. 
The blue color seen on the shank should be run out to the tip; let 
cool on any open surface. The soft broaches usually sold are nearly 
useless. The point is left if canal exploration is intended. For 
carrying cotton twists, cut the end off with scissors. To wind the 



THE FILLING OF ROOT CANALS 



555 



cotton lay a wisp on the left forefinger, lay the broach upon it, close 
down the thumb, then quickly revolve the broach with the right 
forefinger and thumb, pushing the cotton through those of the left 
hand to form a symmetrical cone. To use as a swab, rotate in the 
canal to the right. To leave the cotton in the canal, rotate to the 
right as the twist is pressed to the apex. Then turn the broach once 
or twice to the left to loosen it from the cotton, withdraw a little, 
then press in again. Thus the cotton is crimped upon itself. 

Roots with Open Foramina. — These may be incomplete roots with 
very large apical openings, in which case wax with aristol is the best 
filling used, as previously stated. It should be said again, however, 
that if possible the pulp of such a tooth should be capped to permit 
root formation to be completed. 



Fig. 514 



Fig. 515 




-a 



Manner of measuring the length of a root 
and fitting a gutta-percha cone. 




■a 



Manner of tapering a canal to fit 
cone of the same size. 



- -L> 



If the foramen is of moderate extent and either natural or unfor- 
tunately made with drills, gutta-percha cones are valuable. To 
determine the size of the cone, one of two methods may be employed. 
Perhaps the more accurate is the employment of a series of gradually 
increasing sizes of canal pluggers. One should be selected which will 
just fit the apex or be a trifle too large. By placing this in the hole of 
a draw plate, a specially rolled cone or even a slightly tapering size 
may be made to fit the hole in the plate. The canal is moistened with 
eucalyptol or chloro-percha and a quarter-inch section of the cone is 
carried on the plugger to its place in the root-canal apex. A slight 
protrusion is not ordinarily productive of injury. A cardboard per- 
forated by the respective plugger will do instead of the draw plate. 
If the root length was previously measured with a piece of rubber 
dam slipped over the plugger shank and some known point on the 



556 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

tooth used as a guide, the cone should be seen to go down until it 
chokes the foramen, when the dam should be above the guide point 
a distance equal to the length of the cone section used. 

In the second method a long, tapering cone is prepared. Some 
point on this must fit the foramen. It is tried in and as often as 
sensation is felt it is cut off a trifle and tried again until it chokes 
the foramen without sensation. 

In case of abscess, especially if filling is a means to a cure, this 
may extend beyond the apex of the tooth. 

The cone should be marked at a point corresponding to the guide 
point chosen and be laid aside. Next, a fine hook made by bending 
the tip of a fine broach to a right angle, then cutting it close to the 
shank, has a piece of rubber dam slipped over it and is passed through 
the apex and hooked upon the edge (Fig. 514). The dam is slipped 
to the chosen guide point. The probe hook is withdrawn, the dam 
laid at the mark on the cone, and the cone cut off at the lower edge 
of the hook (Fig. 514, 6). In use, a little solvent, preferably chloro- 
percha, is placed in the canal and the cone slowly slipped to place 
until the mark coincides with the guide point. The cone is then cut 
off with a hot instrument, warmed, and gently packed into the canal. 

When the canal has been reamed with a small engine reamer, and 
the apex enlarged, the hook may be placed and have a bit of rubber 
dam on it as a guide. Then slip a bit of dam over a larger tapering 
root reamer at a corresponding length. Drive the reamer in until at 
the guide point. This gives a tapering cone shape to the canal and 
is a guide in the construction of the cone (Fig. 515). 

In some cases of large foramina or perforation a bit of sterile 
grafting sponge may be introduced into the apical space and the 
filling placed against it. 1 

Canals with Inaccessible Apices. — Any tissue in such apices should 
have been mummified or sterilized with formocresol or be treated 
by Rhein's method 2 of filling a canal with mercuric chlorid in hydro- 
gen dioxid (1 to 500), passing in a zinc probe, then applying the 
anode of a cataphoric outfit with from 1 to 5 milliamperes of current 
from three to seven minutes (the cathode at the cheek). The object 
is to form zinc oxychlorid in the apical root canal through electro- 
lytic action. The canal must be regarded as doubtful, but if well 
opened to the inaccessible portion a trifle of formo-percha may be 
placed on cotton at this point and the balance of the canal be filled 
with antiseptic temporary stopping. The paraform and cassia in the 
formo-percha are active agents. 

1 G. Brunton, England: Dental Cosmos, 1900. 

2 Dental Cosmos, 1905, p. 1196. 



THE FILLING OF ROOT CANALS 557 

A variant consists in the use of embalming paste or Soderberg's 
mummifying paste, either made stiff and introduced with successive 
sizes of pluggers, beginning with the largest admissible and proceeding 
to the smallest, or moistening the canal with the thinner paste and 
packing a cone into it. The use of such a paste in connection with a 
cone of gutta-percha is valuable as an agent embalming the fibrils 
in the dentin of teeth from which living pulps have been removed, 
or of keeping sterile the tubules of those teeth in which the pulp 
is gangrenous (see p. 559). 

If conditions admit of it, provision for future entrance of the canals 
should be made, and it is always well to divide the operation of 
canal filling and crown filling by a short period of time. 

Iodoform paste with or without cotton may be placed in the apical 
third of the canal. 

Root Canals in Temporary Teeth. — These may at times be well filled 
with gutta-percha points, which, if aseptic, do not interfere with 
resorption, but a material of easier adaptation which absorbs with 
the root is preferable. The w T axes meet the indications, as they can 
be pumped while fluid from the action of a hot root drier into all 
inequalities, where they adjust their relation to the soft tissue. 

Buckley recommends in cases of chronic abscess the use of a stiff 
mixture of calcium phosphate and formocresol (formalin, 1 part; 
cresol, 2 parts), to be packed into the pulp cavity and zinc phosphate 
'flowed over it. 

Johnson recommends euca-percha to be pumped into the canals 
and pressure with temporary stopping to be exerted until the solution 
appears at the fistula. Such temporary stopping as does not interfere 
with filling integrity should be left. 

There are various other methods of filling root canals, such as 
driving wood points saturated in carbolic acid into the canals; the 
use of iodoform paste, with or without cotton, or of creosote on cotton 
(preferably raw cotton); the use of balsamo del deserto, etc., which 
have had advocates, but the methods given are those which have 
had long-continued and successful use. 

The Covering of the Root Canal Filling. — The bulb of the pulp 
chamber may be filled with any of the more solid materials. In case 
of a strong crown, temporary stopping makes a good occupant of 
this cavity, though gutta-percha is often used; oxychlorid of zinc 
aids in keeping good color. In the weaker teeth or sometimes for 
other reasons the final filling may extend into the pulp canal to 
assist in anchorage. 

Partial Removal of Pulp.— The Cobalt method of pulp treatment 
has been alluded to. Wm. Herbst, of Bremen, advanced the idea 



558 REMOVAL OF 'DENTAL PULP AND ROOT-CANAL FILLING 

that if the bulbous portion of the pulp be devitalized by cobalt and 
removed, leaving the root portions, the latter will remain vital if 
protected after a manner described by him. The bulbous portion 
of the pulp is cut away and the pulp chamber enlarged by means of 
large rose burs. Over the pulp stumps a cylinder of tin-foil is laid, 
and burnished to fit the floor of the pulp chamber without pressure 
upon the pulp stumps (Fig. 516) . Over this a filling is placed. Herbst 

Fig. 516 




Herbst's method of preserving pulp stumps. 

claims that the pulp stumps will remain vital. Were this to be 
depended upon, it would be a marked saving of time and trouble 
and would lessen the chances of pericementitis subsequent to pulp 
removal; but when it is known that the cobalt of Herbst is metallic 
arsenic, the ultimate death and decomposition of the pulp remnants 
seem almost inevitable, and in fact does occur. The method should 
not be employed. 

MUMMIFICATION OF THE PULP. 

Many experiments have been performed relative to leaving in situ 
portions of pulps and covering them with substances having for their 
object the chemical alteration of the pulp tissue, so that no peri- 
cementitis shall result from its putrefaction. The first effort in this 
direction is credited to Witzel in 1874. 

Miller, 1 after many experiments with various materials, has shown 
that none but the most powerful and penetrating antiseptics have 
value as permanent sterilizers. These are the cyanid, bichlorid, 
and salicylate of mercury, sulphate of copper, and oil of cinnamon. 
Orthocresol, carbolic acid, trichlorphenol, and zinc chlorid penetrate 
the pulp tissue rapidly, but are too diffusible, their effects disappear- 
ing in a few weeks. 

He classifies salicylic acid, eugenol, camphophenique, hydro- 
naphthol, a-naphthol and /3-naphthol, aceticotartrate of aluminum, 
and some essential oils, resorcin, thallin, sulphocarbolate of zinc, etc., 
as being of doubtful value. 

1 Proceedings of Columbian Dental Congress, 1893. 



MUMMIFICATION OF THE PULP 559 

Those nearly or quite worthless are iodoform, basic anilin coloring 
matters, borax, - boric acid, dermatol, europhen, calcium chlorid, 
hydrogen dioxid, sozoiodol salts, tincture of iodin, spirit of camphor, 
and naphthalin. 

The preparation giving the best results consisted of mercuric 
chlorid, 0.0075 gram; thymol, 0.0075 gram, in tablet form. 

The pulp is devitalized; the crown portion and all the root portion 
readily accessible are removed; one of the tablets is placed in the pulp 
chamber, crushed by means of an amalgam plugger, and covered with 
gold-foil. The mercury salt tends to discolor the crown of the tooth, 
so that its employment should be restricted to the posterior teeth; 
indeed, the necessity for its use would be, as a rule, found with these 
teeth, being those from which it is most difficult to extract pulp 
remnants. Miller expresses faith in the power of oil of cinnamon to 
permanently sterilize pulp fragments. 

Soderberg 1 recommended a paste composed as follows: 

1$ — Alum exsic, 
Thymol, 

Glycerol aa 5J 

Zinci oxidi • . . q.s. to make a stiff paste — M. 

It is preferable to add the zinc oxid as needed or to make a small 
quantity of the paste frequently, as it gradually hardens. To the 
paste used a crystal of cocain is added to prevent pain. Bennette, of 
England, has advised the use of paraform incorporated in the paste, 
for its well-known antiseptic and hardening effects. Greenbaum 
suggested the use of a drop of 40 per cent, formaldehyd solution to be 
incorporated with the paste. Both reduce the pulp to the consistence 
of catgut. 

Soderberg reopened cases months after application of the paste to 
pulp stumps, and found them shrunken and with an odor of thymol 
about them. 

He applied the paste in the manner shown in Figs. 517 and 518. 
In 1900 Soderberg reported the use of the paste in about 900 cases, 
of which 220 were test cases of from two to six years' standing. He 
claims that in no case did apical pericemental disturbance arise 
from the use of the paste as described. 

This method has met with much opposition from prominent oper- 
ators, who prefer the thorough cleansing and filling of the canals. 
No doubt the rational method of procedure is to cleanse the canals 
as w T ell as possible, and to use the paste against unremovable pulp 
'stumps. 

While the paste may effect mummification of entire canal filaments 

1 Dental Cosmos, November, 1895. 



560 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

of pulp, leakage is always imminent about shrunken pulps, and the 
only safeguard is the antiseptic effect of the paste. This is much 
enhanced if the bulk of putrefiable material be replaced with the 
antiseptic paste used as a root filling. Many such root fillings have 
done good service for many years. 

Fig. 517 Fig. 518 





a, caries exposing a horn of the a, root portion of pulp; b, mummifying paste; 
pulp. c, zinc phosphate; d, gold or amalgam. 

A certain percentage of failures would be no argument against the 
employment of the method when indicated, as no method is infallible 
in all circumstances, and particularly in those in which the present 
method is indicated. 

Pulp Digestion. — Harlan recommended that the following paste be 
applied to unremoved portions of dead pulps as a means of digesting 
them preparatory to root filling: 

1$ — Papain gr. v 

Price's pure glycerin . Tfl,iv 

Sol. 1 to 200 hydrochloric acid TTlv— M. 

This is applied in the pulp canal, covered with blotting paper 
soaked in liquid vaselin, and the whole temporarily sealed for a few 
days. The pulp is reduced to the consistence of jelly and can be 
readily washed out. 

The method, on the whole, does not seem preferable to either 
mummification or the Rhein treatment or the formocresol treatment 
of inextricable portions of pulps in curved roots, etc., inasmuch 
as the occupancy of a canal by a sterile pulp remnant is better 
than leaving an empty root canal apex or filling only a portion of 
it in such manner as to render subsequent treatment almost im- 
possible. In fact, it is better that dentists recognize their limitations 
and put themselves in position to do future good to the patient, 
than to blindly obstruct efforts in that direction. 

Perforations and Resorptions. — The same accidents that occur in 
canal opening in the case of the removal of anesthetized or devitalized 



MUMMIFICATION OF THE PULP 561 

pulps may occur in all gangrenous cases with somewhat increased 
liability to infection of the pericemental tissue. 

In old cases the pericemental tissue may hypertrophy, causing the 
condition of hyperplastic (fungoid) gum. This should be sterilized 
and burned away with the electric cautery or may be frozen with 
ethyl chlorid and ablated with sharp instruments, or it may be 
saturated with trichloracetic acid and ablated, or it may be pressed 
away (resorbed) with cotton saturated with tincture of iodin or an 
antiseptic oil. The perforation is then covered. 

The Filling of Perforations. — Perforations made high up in the canal, 
after being appropriately sterilized with formocresol, should be filled 
with wax or with gutta-percha cones, which have been accurately 
fitted to the openings. It is often difficult to do this accurately, 
but the effort should be made. When ready, a little antiseptic 
chloro-percha is to be placed in the perforation or upon the cone, 
and the latter packed to place. 

In low perforations without a fistula associated, the opening of 
the perforations should be enlarged inwardly and a ball or plaque of 
aseptic, warm, low-heat gutta-percha, or even temporary stopping, 
adapted to the opening. A piece of pure gold plate may be burnished 
over an accessible opening, and be adapted with thick chloro-percha 
or temporary stopping. Any of these may be fixed in place with 
oxyphosphate of zinc. Quick-setting oxyphosphate of copper in its 
soft, gummy, state may be painted over the tissue and root opening 
by means of an instrument, or the perforation may often be satis- 
factorily closed with copper amalgam. When in posterior teeth a 
pin must be used, the pin may be made smaller than the root canal 
and be coated with wax, soft oxyphosphate of copper is put in the 
canal, and the pin gently thrust in. When the cement has set the 
pin may be heated and withdrawn, and when included in the intended 
superstructure, the pin may be again cemented in place (see Figs. 
378, 381, and 382). 

When a perforation threatens to produce an abscess an artificial 
fistula should be made and the case treated accordingly. 

If a perforation have a fistula associated with it, the oxyphosphate 
of copper or zinc oxychlorid may be allowed to go through the fistula, 
by way of which any excess may be removed. 

In case of resorption of the roots of permanent teeth great difficulty 
may present, the soft, absorbent tissue having grown into the cavity 
in the root side which it has made. A radiograph will aid in deter- 
mining the extent of the lesion, which usually renders canal treatment 
impossible and extraction imperative. 

36 * 



CHAPTER XVIII. 
GANGRENE OF THE PULP. 

Definition. — By gangrene of the pulp is meant its death through an 
interference with its nutrition. It may be partial, as when an abscess 
in the pulp or violent irritation causes the bulbar portion to die, the 
canal portions being found alive; or when only one canal portion is 
dead, the others being alive. Either dry or moist gangrene may occur. 

Causes. — It is probable that a construction of apical root tissue 
(hypercementosis) about the pulp may so constrict it as to bring 
about its death. (For the primary causes of this see Hypercemen- 
tosis.) Sudden shocks, such as occur from thread, string, or cigar 
biting, or blows or rapid movement in regulating or wedging, or 
non-fixation after regulation, may cause torsion or tension of the 
bloodvessels entering the apex of the pulp. 

These influences may either cause pulp hyperemia or strangulation 
of the apical bloodvessels, or, possibly, an area of apical thrombosis, 
cutting off the nutritive supply to the pulp. Septic or aseptic inflam- 
mation of the pulp may cause its total death. Death of pulp tissue 
due to arsenic produces results in nowise differing from gangrene, 
provided the pulp be left in situ. (See p. 521.) 

DRY GANGRENE OF THE PULP. 

Definition. — By dry gangrene of the dental pulp is meant its death 
in toto and its subsequent transformation into a dry, shrivelled mass 
occupying the pulp chamber and canal. 

Causes and Pathology. — If the pulp die and remain under conditions 
which exclude bacteria from contact with it, the water of the pulp 
may be removed, leaving the organ as a tough, shrivelled mass (Fig. 
519). The conditions most favorable seem to be: (1) Pulp death 
from some aseptic cause, e. g., the hyperemia resulting from a blow 
on a sound tooth; (2) constriction of the apical foramen, due to hyper- 
cementosis, the result of thread biting or other mild irritation of the 
pericementum; (3) the presence of secondary dentin over the bulbar 
portion of the pulp, causing pulp exhaustion yet protecting it from 
infection; (4) the capping of the pulp with zinc oxychlorid or formagen 
paste, the pulp being permeated with the drug or dried by it; (5) the 
(562) 



DRY GANGRENE OF THE PULP 563 

covering of pulp stumps with a paste containing a tannifying sub- 
stance, such as alum, formaldehyde, or tannin. 

The water necessary to putrefaction is abstracted, either naturally 
or chemically, and probably bacteria are at the same time excluded, 
either mechanically or because the chemical substances used have 
penetrated the pulp tissue, acting as antiseptics. 

Symptoms. — The tooth has a nearly normal color, but under a 
reflected light is seen to have lost perfect translucency. There is no 
response to thermal or electric tests for pulp vitality. The dentin is 
insensitive to cutting instruments, and the cuttings upon the bur 
have no odor. There is no odor or fluid in the pulp canal .when this 
is entered, and the pulp is found as a tough, dry mass not unlike 
that seen in a dry extracted tooth which contained a vital pulp at 
the time of extraction. These cases as spontaneous occurrences are 
relatively rare. 

Tests for Pulp Vitality. — The diagnosis of pulp vitality or death 
being in practice almost daily required, the decisive tests are here 
indicated. 

A tooth containing a vital pulp is translucent and pink; that con- 
taining a dead one always opaque to transmitted light, and usually 
clouded to a gray or bluish black. The ordinary appearance by 
reflected light often corresponds to this, but sometimes a tooth is 
clouded by fillings, or looks dead, but is vital. 

An electric mouth lamp with or without a reflector so arranged as 
to reflect the light upon the lingual surface of the tooth will supply 
the means for this test. In its absence strong sunlight may be 
reflected by means of a mouth mirror, but is not nearly so good a 
means as the electric light (Fig. 369). 

If the tooth be isolated by means of rubber dam and, first, cold 
water be thrown, or, later, ethyl or methyl chlorid be sprayed upon 
it or upon the filling contained in it, absence of response will indicate 
either partial or total pulp death or the formation of a quantity of 
secondary dentin. In the latter case the test must be renewed 
as the excavation proceeds. 

A hot burnisher or hot gutta-percha applied to a filling or dentin, 
or very hot water thrown upon an isolated tooth, should provoke at 
least a delayed response from a' vital pulp. 

The application of a small high frequency glass electrode to the tip 
of a vital tooth produces a peculiar sensation not unlike that of 
hypersensitive dentin. It is due to the fact that the enamel is like 
glass unable to insulate the high frequency current which passes to 
the dentinal fibril. A devitalized tooth will not respond. The 
facility of this test makes the apparatus a very valuable time saver. 



564 



GANGRENE OF THE PULP 



It is well to take up the current with the fingers on the side of the 
tube at first and to raise the finger after the glass is in contact with 
the tooth. 

Woodward has shown that if a few cells of a cataphoric apparatus 
are in action and the positive electrode be applied to the dentin or 
metal filling in a vital tooth, while the negative pole is at the cheek 
or wrist of the patient, a distinct sensation should be felt, while in 
case of a dead pulp there will be no response; usually even a small 
filling will transmit a distinct shock in a vital tooth which is absent 
in a devitalized tooth. A mild interrupted current has also been used 
for the test. There may be no response through a metal filling, while 
such response may be obtained by packing wet cotton against the 
dentin after some drilling. A mild current should always be used 
unless there is no response, w T hen the strength of the current should 
be increased. It is generally possible to test some evidently vital 
tooth nearby as a control. If the filling reach the gum, the current 
may be transmitted by it. The possibility of contact of the filling 
with another in a vital tooth is to be remembered. Insulation with 
rubber dam is indicated in such a case. 



Fig. 519 



Fig. 520 



Fig. 521 






Dry gangrene of the 
pulp: PN, pulp no- 
dule; DP, shrivelled 
pulp. (From a speci- 
men of pulp extracted 
intact in this con- 
dition.) 



Caries; moist gangrene in impris- 
oned temporary molar. (Skia- 
graph by Hagopian from editor's 
case.) 



Moist gangrene. 
Skiagraph of unfilled 
root canals with large 
mass of filling mater- 
ial built in over them. 
(Price. 1 ) 



In doubtful cases, such as that shown in Fig. 521, the axray skia- 
graph is valuable, and indicates at least the removal of the filling for 
further diagnosis and treatment. When dentin is insensitive, pulp 
death should be suspected. 

A strong odor of putrefaction may be obtained from bur cuttings 
in cases of moist gangrene only. This must be differentiated from 



Items of Interest, 1901. 



MOIST GANGRENE OF THE PULP 565 

the odor of decayed dentin, which usually also has an acid character. 
In case of partial death of the pulp not discoverable by the tests 
given above, a fine, sharp probe passed into contact with the pulp 
remnant will demonstrate its vitality. 

Treatment. — If septic matter be introduced a violent pericementitis 
may be lighted up; but if aseptic precautions be employed in opening 
the canal, and this be kept under the influence of a germicide, such as 
5 per cent, formaldehyde or sodium dioxid, the root may be filled. 
A dressing of formocresol may be introduced for a time and the 
root then filled. 

A temporary filling of pink base-plate gutta-percha is to be inserted 
in the crown cavity until all irritation, if any, subsides. 

Slight aseptic apical irritation may be anticipated as a matter 
of precaution by the use of iodin as a counterirritant at the time 
of root filling (see p. 476). Such irritation is either mechanical or 
due to the chemical substances used. 

MOIST GANGRENE OF THE PULP. 

Definition. — By moist gangrene of the pulp is meant death of pulp 
tissue en masse and its subsequent decomposition by the action of 
putrefactive agencies. As putrefactive decomposition is the essential 
feature in these cases, and that which gives the process its patho- 
logical significance, the causes, nature, effects, and treatment of 
putrefactive decomposition of the pulp are included under this 
subheading. 

Causes. — The causes of moist gangrene are such as may cause the 
death of the pulp and its subsequent decomposition by bacteria. 
Without bacteria putrefaction cannot occur. Among these the 
Bacillus gangrense pulpae (Arkovy) figures prominently. 1 Four types 
of cases are seen: (1) In teeth apparently sound; (2) in teeth filled, 
but the canals not treated — i. e., death of the pulp has occurred after 
filling; (3) in teeth filled with canals partly filled; (4) in teeth having 
open cavities and canals. 

In the first type of cases the bacteria may enter by way of the 
blood channels, but it is not improbable that slight cracks or histo- 
logical defects in the enamel may admit to the dentinal tubules the 
necessary bacteria, or that they may gain entrace by way of the 
cementum and dentin at the neck of the tooth. (See Caush's Tubes). 
.The inference is similar in case of trimmed crowms of teeth underlying 
gold caps. 

1 Siberth and Goadby regard this microorganism as a variety of Bacillus mesen- 
tericus, probably "niger. " Mycology of the Mouth, p. 148. 



566 



GANGRENE OF THE PULP 



Pigment. 



Fig. 522 
Sulphur + hemoglobin. 



A case presenting some analogy to these teeth is that of an egg with 
apparently perfect shell, but in which intense decomposition has 
occurred. That the gases and other odorous products are somewhat 
confined the author proved to his dismay as a boy by smashing with 
a hatchet one found in the brush. 

Many of these teeth do not develop abscesses even after the tooth 
has become dark in color; perhaps the bacteria are killed by their 
own products. If the dentin be exposed, as at the incisal edge, the 

abscess may develop. The en- 
trance of air or beginning of 
treatment often starts an abscess 
unless treatment is instituted. 

In the filled cases crevices 
about crown and root fillings 
may admit bacteria, which may 
pass through the tubules of even 
secondary dentin in some 
amount. On the other hand, 
it is irrational not to admit the 
possibility of an infection via the 
circulation. 

In cases of obvious pulp infec- 
tion beneath fillings — e. g., sup- 
puration of the pulp — the bac- 
teria necessary are in situ. 

In the open cases the infec- 
tion obviously arises from the 
mouth. 

Pathology and Morbid Anatomy. 
— The pulp being wholly or 
partly dead from any cause 
whatever, saprophytic bacteria 
gain access to it, and the 
serial decomposition it under- 
goes is in exact correspondence 
with that of moist gangrene or putrefaction in other localities. 
In this serial decomposition albuminous substances are first trans- 
formed into peptones and allied substances, some of them being 
very toxic. Compound ammonias, known as ptomains, or animal 
alkaloids, such as putrescin, neuridin, and cadaverin, are probably 
next formed. Next the nitrogenous bases — leucin, tyrosin (amido- 
acid), and the amines (methyl, ethyl, and propyl) — make their 
appearance, together with organic fatty acids, Next aromatic 




C0 2) NHa; 
H 2 and H 3 S. 



Aromatic and 
fatty prod- 
ucts. 

Ptomains. 



Peptones. 



Diagram illustrating the more com- 
plete decomposition of the pulp at its 
coronal end. 



MOIST GANGRENE OF THE PULP 



567 



products, indol, phenol, cresol, etc., and finally hydrogen sulphid, 
ammonia sulphid, carbon dioxid, and water. By alternating pro- 
cesses of hydration, reduction, and oxidation, bodies of increasing 
simplicity of chemical composition are formed. "Fermentation and 



Fig. 523 




Fig. 526 



Fig. 527 





Fig. 528 
f//'l 



Fig. 529 



>M)<0 



'V 



f /". 



Fig. 530 






»• \ 



putrefaction can only occur where the fungi concerned live and the 
extent of decomposition is conditioned by the number of fungi." 1 
The contents of the tubules (fibrillar) also are putrefied. These 



1 Ziegler: General Pathology. 



568 GANGRENE OF THE PULP 

products are derived from the following chemical constituents found 
in normal pulps, according to Hodgen: Proteins and albuminoid, 
fibrin, hemoglobin, collagen, elastin, fats, tripalmitin, stearin, and 
olein. 

The irritant bodies are probably the gases and ptomains which 
have experimentally been found capable of producing suppuration in 
the absence of bacteria. 

Miller 1 found, in the deepest portions of the degenerating, putrefy- 
ing pulps, w T here inflammation and suppuration were in progress a 
preponderance of small cocci and diplococci, and proceeding toward 
the open pulp chamber an increasing number of large cocci, several 
forms of bacilli, vibrios, and other spirillar, spirochete, and long 
thread forms (Figs. 523 to 530). Figs. 529 and 530 are from the same 
pulp; Fig. 524 was taken from the radicular portion of a pulp which 
was alive and suppurating; Fig. 529 was from the putrid crown por- 
tion. Miller found that bacteria of pulp putrefaction cultivated in 
gelatin, with and without the access of air, exhibited a difference in 
the poisonous properties of their products. Those developed with 
free access of air produced stronger reaction, and more extensive 
suppuration than those developed without the access of air. 

Arkovy, 2 in an examination of 43 cases of chronic apical abscess, 
pulp gangrene, etc., found the Bacillus gangrense pulpse present in 
41; the Staphylococcus pyogenes aureus in 15; Staphylococcus 
pyogenes albus in 8; Staphylococcus pyogenes citreus in 2; Strepto- 
coccus pyogenes in 10, and Bacillus pyocyaneus in 4. 

He found the Bacillus gangrense pulpse in mouths free of caries as 
well as in mouths containing carious teeth, and established the fact 
that it is pleomorphous (bacillus and coccus form). 

He inoculated healthy pulps with this bacterium, and found that in 
pure culture it produced total gangrene without suppuration; while 
mixed cultures, and even the mixed pleomorphic forms of the same 
bacillus, produced chronic pulpitis. 

On gelatin cultures a putrid, cheese-like odor was perceptible. The 
germ is subject to the antiseptic effects of strong acids, alkalies, car- 
bolic acid, and tincture of iodin, which explains, in part, the success 
of the treatment hereinafter mentioned. 

Arkovy's demonstration seems a satisfactory explanation of cases 
of quiet death of pulps under fillings. 

The hydrogen sulphid combines with the HN 3 of proteid origin, 
to form ammonium sulphid (NH^S, which, again, combines with 
the iron in the hemoglobin of the red corpuscles, producing ferrous 

1 Dental Cosmos, 1894. 

2 Synopsis by Soderberg: Dental Cosmos, 1899. 



MOIST GANGRENE OF THE PULP 569 

sulphid, Fe2S, which darkens the decomposing tissue, and, entering 
the tubules, stains the dentin a slate-gray or bluish-black color. 
Other derivatives of hemoglobin may be responsible for the yellowish 
brown discoloration often seen in cases in which bacteria have not 
reached the pulp until long after pulp death. The color is, therefore, 
not due to the presence of hydrogen sulphid. 

Miller 1 found that the reaction in cases of putrefaction was alkaline 
unless a certain percentage of sugar was introduced into the medium, 
when it was acid. He explains the voluminous foul odor of confined 
dead pulps as due to the absence of oxygen of air. If present as in 
open pulp cavities the gases escape, the volume being therefore 
reduced, oxidation of gases increased, and an acid reaction due to 
entering carbohydrate permitted. The exact nature of pulp decom- 
position is in some doubt. 

Fig. 522 is a diagram illustrating these changes; it being assumed 
that the decomposition is most advanced at the crown portion of the 
pulp, owing to the entrance of bacteria at that point. 

In the early stage of the process the gangrenous pulp resembles 
a yellowish mass of sloughing tissue, with reasonably tough con- 
sistence, which can be easily removed. In the later stages it is more 
decomposed and dark and jelly-like, and yields to the broach. 
Naturally the greatest number of fungi will have, by multiplication, 
invaded and putrefied that end nearest the source of infection, while 
the more consistent (less putrefied) portion of the pulp will exist 
at the apex. In the final stages nothing but fluid, or even an almost 
dry canal, may be found. This last condition must not be con- 
founded with dry gangrene. If fluid, or odor without fluid, be 
present the case is one of moist gangrene. 

Gangrenous pulps do not necessarily produce abscesses at once, 
but often clinical history shows that a year or two, or even more, 
may elapse, though as short a time as two or three weeks has some- 
times been sufficient. In one case of a boy, aged ten years, the time 
between a capping of a bleeding pulp with Jodoformagen and the 
presence of a fistula upon the gum was but two weeks. It was, 
however, in a temporary first molar, and the cement covering the 
cap was found to be loose. 

The forcing of gangrenous pulp tissue by instrumentation into 
apical tissue generally results in an abscess, even when extraneous 
bacteria are presumably not introduced. 

The irritating substances in a decomposing pulp are presumably 
the bacteria, the ptomains, and the expanding gases. 

1 Microorganism of the Human Mouth, 1890 



570 GANGRENE OF THE PULP 

Many decomposed pulps produce no pain, but in these cases 
the gases may escape via dentinal tubules and leaks about fillings 
(Fig. 521). 

Clinically, putrefactive pulps may be found in sound teeth, in 
filled teeth, and in teeth the pulp cavities of which are open to the 
oral fluids, either actually or through the medium of open tubules 
in the dentin over them, or in apical portions of poorly cleansed or 
partly filled canals. A cotton dressing having a bad odor, or an 
apparently empty apical portion of canal or a leaky gutta-percha 
canal filling associated with a bad odor, even though the pulp has 
been successfully removed, have a similar pathology. There is 
little difference in principle between putrefactive serum or tubule 
contents and a putrefactive pulp. Any of these may cause abscess 
or remain quiescent. 

Symptoms. — The symptoms are opacity of the tooth evident to 
the eye or noted by transmitted light, bluish or brownish discolora- 
tion of varying degrees, odor, and discoloration of the dentin in a 
cavity. 

There is a lack of response to cutting, thermal, and electric tests. 
Sometimes a bad taste due to leakage about fillings is present. Upon 
drilling out a filling the odor of putrefaction may be clearly noticed 
even before entrance of the canal, and sometimes rises to the operator's 
nostrils. The odor of the bur cuttings is diagnostic in less pronounced 
cases. The gases may be present in quantity without symptoms of 
pain. Looseness, tenderness to percussion, incipient and acute 
abscess, or a chronic fistula are evidences of pericemental irritation. 

Pain to heat, while usually indicative of pulp irritation, also some- 
times occurs, and is explainable upon the same theory of the expan- 
sion of gases against vital tissue — in this case the apical tissue. These 
symptoms are all explained by the pathology of the condition. 

A confusing condition clinically is found where one-half of a pulp 
has died and undergone decomposition, as in molars, the other half 
remaining vital, although the seat of infection and inflammatory 
action. So far may this condition go, that abscess, acute or chronic, 
may be present upon the root of one tooth long before the second 
segment of the pulp has succumbed. The diagnosis of such cases is 
made by the light test, by obtaining the painful reaction to heat and 
perhaps to electricity, and usually some tenderness upon percussion 
upon some particular portion of the tooth; upon opening the tooth 
the peculiar condition described is found. The x-rays should show 
the condition. 

In one case of a lower molar with a fistula related with the distal 
root I found the pulp apparently vital upon entering the pulp chamber 



MOIST GANGRENE OF THE PULP 571 

with a bur at a point about midway between the horns. There was 
apparently a persistence or hypertrophy of the pulp bulb attached to 
the mesial filaments. The distal canal was found to contain only the 
fluid remains of a dead pulp filament. In cases seen at the right 
time the bulbal half of a pulp may be gangrenous without positive 
putrefaction, while the apical half is still vital. 

J. H. McQuillen 1 recorded a case of longitudinal fracture of a 
bicuspid tooth extending from the sulcus to the bifurcation of the 
roots, and which was apparently due to the expansion of the gases 
of decomposition. Poinsot 2 records a similar case, and states that 
several teeth containing decomposed pulps confined in a glass tube 
caused the latter to break. 

Fig. 531 




Tooth split by gas. (Roff.) 

Dr. S. H. Roff, 3 of Cincinnati, Ohio, has presented the case shown 
in Fig. 531. He had it under observation for seven years. He 
regarded the case as one of slow progressive cracking (a run) with 
final irritation and death of the pulp and the final clean longitudinal 
fracture as due to the gases from the partially decomposed pulp. 
When one considers the fact that wet plugs of soft wood will split 
granite boulders we must accept the possibility of tooth fracture 
by gas pressure. 

Observations previous to that of McQuillen have recorded a sound, 
as of an explosion, to have occurred simultaneously with the fracture 
of the tooth. I have looked all my professional life for such a case, 
but though I have seen quite a number of clean fractures I have 
never been able to eliminate the possibility of fracture from ordinary 
causes and in some of the cases have had positive histories of direct 
violence. 

Treatment. — The pulp being presumably infected, all quiescent 
gangrenous pulps or putrefactive conditions under any conditions 

1 Dental Cosmos, 1871. 2 Ibid., 1901. 

3 Items of Interest, March, 1912. 



572 GANGRENE OF THE PULP 

discovered indicate a similar treatment, namely, first disinfection to 
remove or kill bacteria which might cause an abscess and at the 
same time to destroy the chemical nature of the gases and ptomains. 
After this the canals are to thoroughly opened, cleansed, further 
disinfected for the sake of surety, and later filled. 

Three substances are preeminent in this direction — (1) formal- 
dehyd, (2) nascent oxygen, (3) iodin or its derivatives. 

At the present writing no substance equals formaldehyd, because 
of its rapid diffusion as a gas through all canals, tubules, and even 
abscess tracts. 

The first and best treatment consists in opening the pulp cavity and 
gently removing the bulk of decomposed pulp from the pulp chamber 
and canals, care being employed to avoid forcing any putrid material 
into the apical tissue by broaching or plunging of the bur. Also, no 
bacteria should be introduced from outside. The opening should not 
be too freely made, and should be funnelled or countersunk out- 
wardly to secure the seal against being plunged into the pulp cavity 
in mastication (Fig. 532). 

This being done, the canals are dried with cotton and hot air, and 
a small pellet of cotton saturated with formocresol or 10 per cent, 
aqueous formaldehyde solution, or geranium formol 1 is to be placed 
in the pulp chamber. 

1$ — Formaldehyd 40 parts 

Essence of geranium, distilled 20 parts 

Alcohol 80 per cent 40 parts 

Any that has come in contact with the orifice should be removed 
with alcohol. The orifice is then dried and a small piece of dry spunk 
placed over the application, but not so as to interfere with the 
seal. Quick-setting, adhesive, hydraulic cement is now flowed into 
the orifice, air bubbles being avoided by flowing it in with an instru- 
ment (Fig. 532). A bit of paraform accomplishes the same purpose 
as the solution, namely, the liberation of formaldehyd gas. 

When opportunity for self -relief seems proper, as when the operator 
is leaving his practice for a short time, or may otherwise be inacces- 
sible, hot temporary stopping may be used and the patient instructed 
as to the proper procedure 'to obtain relief. An ordinary pin crooked 
at the point by striking it across any hard surface will serve to pick 
out the stopping and cotton. In all cases tight coverings must be 
made, as the object is to concentrate the action of the formaldehyd 
gas upon the canal and tubular contents. 

In some cavities it is well to make the covering first, as done for 

1 Geranium-formol introduced by Andre and de Marion, l'Odontologie; abstract 
by International Dental Journal, 1901. 



MOIST GANGRENE OF THE PULP 



573 



arsenic (see Fig. 453), and to seal the dressing in with a further 
addition of cement or temporary stopping. The latter does not 
permit mastication like the former. 



Fig. 532 



Fig. 533 





a, cotton and formocresol; b, spunk: 
c. cement. 



Cervical wall built up with amal- 
gam to permit canal sterilization 
and treatment. 



If there be a broad cavity extending beneath the gum, it is well 
to press the gum away with cotton pellets, then to form the cavity 
and open the canal orifices. Then a retention at the cervical portion 
of the cavity should be made, even if it be necessary to drill a series 
of pits along it with a No. 1 bur. Spunk is now placed over the 
pulp canals and quick-setting amalgam is to be permanently built 
in at this part of the cavity. When set the spunk is withdrawn, 
formocresol in cotton is placed instead of the spunk, and the covering 
completed with cement. The amalgam is finished as far as practi- 
cable at the one sitting, and the case dismissed. At future sittings 
the rubber dam may be applied and the canal work done (Fig. 533). 
When cavity walls are frail, spunk ma}' be placed in the pulp cavity, 
and a permanent cement lining built into the cavity. This can be 
perforated to the spunk, thus leaving the walls supported during 
the treatment. 

Formocresol, introduced by Buckley, consists of equal parts of 37 
per cent, aqueous formaldehyd solution and cresol, which combine 
well. 

According to Buckley, the formaldehyd not only acts as a germi- 
cide, but combines with the ammonia of ammonium sulphid to form 
urotropin and water, 6CH 2 + 4NH 3 = (CH 2 ) 6 N 4 + 6H2O, and 
with hydrogen sulphid to form sulphur and methyl alcohol, 2CH 2 + 
2H 2 S = S 2 + 2CH3OH. The cresol is supposed to act. upon the 
fatty compounds, changing them into a compound resembling lysol. 
Thus, antiseptic substances are formed from poisonous ones. This 
does not necessarily represent all the reactions occurring, as many 
other compounds may result from putrefaction. The probability is 



574 GANGRENE OF THE PULP 

that the thoroughly bactericidal action is the one of greatest value. 
This action has been shown by Mayrhofer to be true only for the 
first twenty-four hours; thereafter the bacteria in the tubules may 
grow back into the canal and the dressing, in spite of the fact that 
the odor of the dressing is present. The canal should therefore be 
mechanically cleaned after twenty-four hours, and a fresh application 
be made. 1 Mayrhofer claimed inability to sterilize permanently 
with formocresol. Nevertheless the editor treats such cases at wide 
intervals ordinarily with impunity. In a few cases an abscess has 
supervened after the first dressing, but none as yet after the second. 
Leakage of the formaldehyd gas may have been the reason, but a 
chronic apical abscess in the third stage (which see) has been a 
suspicion. Cleansing and reaming the canals at the first sitting is 
another danger, even when formaldehyd is subsequently used. This 
must sometimes be done as when a crown is broken away and the 
root canal is foul. 

Formaldehyd is so efficacious in the writer's hands that it has 
displaced other methods in his practice. All other methods of 
disinfection produce results less certain than those produced by it, 
and are more cumbersome, therefore they will be here dispensed 
with. While this is true for a great majority of the cases, occasionally 
a patient is met with whose tissues do not tolerate formaldehyd 
well. Formocresol then should be reduced to a 5 per cent, solution 
with cresol or phenol camphor, and in some cases abandoned for 
more sedative antiseptic remedies, such as eugenol or phenol camphor 
with menthol or thymol or iodoform may be tried. 

This first dressing may be left for from twenty-four hours to a week 
or longer if the patient is comfortable. 

At the second sitting the rubber dam is to be applied and the canal 
opening thoroughly made under formocresol influence, just as though 
the pulps were vital, the technique differing in no respect. (See 
pp. 532 to 548.) A second dressing is introduced into the canals. 
Whether this shall carry the full strength formocresol or it shall be 
modified by the addition of cresol or phenol camphor depends upon 
the history of any irritation or perfect comfort as a result of the 
first application. The object of a second dressing is to determine 
whether the odor (gases) has been discharged from the tubules. 
When the dressing has absence of putrefactive odor, no pus can 
be detected, and the patient is comfortable, the canal is ready for 
filling. Less than this result is too soon, and delay beyond this is 
a loss of time. 

1 Viuileumier : Items of Interest, March, 1910. 



MOIST GANGRENE OF THE PULP 575 

When one pulp filament is gangrenous and another vital, the treat- 
ment is the same, it being the writer's experience that formocresol 
loosely placed is not incompatible with ulcerated pulps, and, indeed, 
is an excellent dressing for suppurative pulps when modified to a 3 
to 5 per cent, strength; even full strength has been acceptably used. 
Later, the vital portion is appropriately removed. 

When apical pericementitis of a subacute nature is present on a 
filled tooth, as when a tooth shows some looseness and tenderness, 
with some injection of the gum, all faulty root canal fillings should 
be removed with barbed broaches, cleansers, or root reamers, and 
the case is then resolved into one of moist gangrene and treated 
accordingly. 

Wax may be removed by over heating with the hot root drier and 
absorption with cotton, or oil of cajeput may be used as a solvent. 
Paraffin may be removed in like manner, xylol is a solvent. 

If a cotton root filling be found it sometimes allows the broach to 
tear loose. In such case a Kerr broach is driven into it to create 
a central opening, after which the fibres become engaged by the 
barbed broach. 

Eucalyptol or chloroform may be used to soften gutta-percha root 
canal fillings, and at times the smallest Kerr or Downie broach is to 
be bibevelled at its end and used as a drill, cutting its way. Oxy- 
chlorid and other cement fillings may have 50 per cent, sulphuric acid 
or strong ammonia water applied to them to assist in breaking up 
the bond of the cement by chemically destroying either the zinc 
oxid or the acid. The drill will tamp the fluid into the cement 
and cut the cement at the same time. 

All root fillings of cement nature are apt to be faulty when used 
as such, because the air in the canal prevents ingress, though it 
may appear to be well filled. This fact is of importance in diagnosis 
in filled teeth, giving evidence of chronic pericementitis, i. e., there 
is probably an unfilled portion of root canal containing putrefied 
pulp or serum. 

It is a weakness of many good operators, if not all, to think that 
their individual canal fillings are perfectly made. The writer was 
once associated with a most conscientious man, and possesses a gutta- 
percha canal filling of his in a molar now successful for twenty years. 
On one occasion he declared that he had filled perfectly a canal of 
an upper second bicuspid, because the material had been felt by the 
patient as it reached the apex. Two weeks later the tooth was 
extracted, though comfortable, for orthodontic purposes. Its well- 
opened canal was empty for a quarter of an inch at the apex. 

To remove pins from roots a bibevelled Kerr broach may be driven 



576 GANGRENE OF THE PULP 

into the cement or dentin about it and the drifts united. The pin 
may often be forced to one side and then jigged loose. If there be 
sufficient pin extending above the face of the root a "pin puller" 
may be used. If the pin cannot be loosened it must be drilled out 
bodily. A sharp round bur should be used to countersink the end of 
the pin, and then by the aid of oil it is cut into shavings. Frequent 
desiccation and examination to observe the presence of a metal 
remnant is necessary to avoid the accident of perforation. 

In drying with the compressed-air syringe, care should be employed 
to avoid extensive emphysema of the cheek, which may be induced 
by intense pressure. If it occur, the emphysema should be reduced 
by manipulation, with a view to gently forcing the air back through 
the root. Christensen 1 and L. Greenbaum have each reported a 
case, and the editor had his first case when desiccating an accidental 
lateral perforation. This occurred even without close application 
of the syringe nozzle, 35 pounds pressure being used. 

Another case occurred while an upper lateral with large apical 
foramen and even with an open fistula was being dried out. The 
entire right cheek and lower eyelid was instantly puffed up. The 
patient called attention to a stiffness and coldness. It subsided 
upon manipulation. There might be dangerous sequelae if sepsis were 
present. 

The immediate treatment of canals containing gangrenous pulps 
may at times be necessary. The mechanical work should be done 
while the canal is flooded with formocresol, and embalming paste 
containing paraform should be used with gutta-percha canal points, 
or sometimes on cotton twists. 

If any inaccessible portion of root canal remain it may be treated 
according to Rhein's method. (See p. 539.) 

Root sterilization may be immediately attempted after the rubber 
dam has been placed and the crown washed with 5 per cent, formalin 
or alcohol and water. 

A little dry sodium dioxid is placed upon a slab with a drop of 
water near it. A broach is drawn through the water, then through 
the powder, and the adherent powder carried to the canal and gently 
passed into the moist putrid contents of the canal; a reaction occurs 
between the water and sodium dioxid as follows: Na 2 02 + 2H2O = 
H2O2 + 2NaOH, producing hydrogen dioxid and sodium hydrate. 

The sodium hydrate or lye saponifies all fatty matters and destroys 
organic matter, even living matter, and the hydrogen dioxid liber- 
ates nascent oxygen, which is a disinfectant. No oil or phenol 

1 Dental Cosmos, 1904, p. 151. 



MOIST GANGRENE OF THE PULP 577 

should be used with dry sodium dioxid, as an explosion may occur. 
The use of the alloy kalium natrium in a moist canal causes an 
oxidation of the metals by the O of the water, flame being the result 
of ignition of the hydrogen. Sodium and potassium hydrate are 
formed. 

The result of the reaction should be washed out with a gentle 
stream of warm water, while a broach is gently passed to and fro 
through the mass. The action is then repeated as far as it can be 
carried. 

The danger in the use of these materials lies in the possibility of 
the production of a chemical inflammation of the apical tissue, due 
to the nascent hydrates, if the foramen be open, winch inflammation 
may be severe, or in the possibility of a non-sterilization of the 
contents of inaccessible canals. For this reason it may be well in 
fine roots to follow^ with the Rhein method, or to use a formalin 
solution for the purpose of completing the sterilization in the more 
open roots, and 20 per cent, formalin or 25 per cent, ethereal pyro- 
zone (H 2 2 ) for the finer roots. 

Following this the root filling is either attempted immediately 
with removable antiseptic root fillings or a dressing of 5 per cent, 
formalin introduced into the dried canal for a few days. 

Any irritation of chemical nature may be treated in anticipation by 
the use of counterirritants applied to the gum. While this may be 
done in some cases the occasional production of an abscess leads the 
editor to strongly advise the first treatment suggested. The writer 
on a Monday lanced an acute abscess on a cuspid treated with kalium 
natrium by a clinician at a clinic on Saturday. Opening the canals 
under antisepsis with formocresol kept in them while broaching, 
etc., is an even better immediate method, but still not so good as 
twenty-four hours' sterilization, then free opening. 

The filling of canals by driving wood points saturated in carbolic 
acid into the infected canals, forcing carbolic acid by pressure into 
the apical tissue, and the filling with gutta-percha are all successful 
in many cases; but there is much likelihood of apical abscess, or, at 
least, of traumatic or chemical irritation, which it requires much 
courage not to undo, with a patient complaining, and some doubt as 
to whether an abscess will result, so that more gradual yet thorough 
work is advisable, at least for the young practitioner who must 
retain the confidence of the patient. 

, Hoffendahl, 1 of Berlin, has extended the demonstration of Zierler 
and shown that the constant galvanic electric current from a battery 

1 Dental Cosmos, 1905. 
37 



578 GANGRENE OF THE PULP 

of from 30 to 40 Leclanche cells to overcome the resistance of the 
tissues will electrolytically decompose 0.75 per cent, sodium chlorid 
solution and drive nascent chlorin, H2O2, and oxygen through even 
fine root canals and into the infected tissue about an abscess cavity. 
Thus, electrolysis and cataphoresis are brought into play. The 
current does not pass through the side of the root; a street or central 
direct current with a rheostat attachment reducing the current to 
from to 80 volts is equally effective. 

The tooth should be rubber dammed to insulate the gum. The 
canal should be carefully cleansed, so as not to permit ptomains to 
pass into the apical tissues, and then filled with a sodium chlorid 
solution. A fine platinum electrode is introduced into the moist 
canal, and must be attached to the positive pole of the battery. A 
large moist negative electrode is to be applied to the hand to lessen 
resistance and conduct the current to the negative pole of the battery. 
The size prevents uncomfortable sensations about the tooth. The 
rheostat should be manipulated so as to introduce the current gradu- 
ally until about 1.5 mi. is recorded on the meter, and should be 
continued for five minutes. An antiseptic dressing is then inserted, 
and a few days later the current is repeated to destroy any bacteria 
developed in the interim, when the root may be filled. Hoffendahl 
employs a paste of paraform, thymol, oil of cloves, and zinc oxid 
packed by means of asbestos fibres. 

In experiments in conjunction w T ith W. D. Miller they found 0.6 
mi. passed for ten minutes through a putrid pulp to which pure 
cultures of germs were added, sterilized the pulp so that agar cultures 
failed; canals of multirooted teeth are best treated separately. 

The principle involved in immediate sterilization is the destruction 
of all septic matter within the canal and beyond the apex at the 
first sitting. 

After the canal disinfection is accomplished by one or more of the 
various immediate means suggested, its walls should be desiccated 
and made absorbent by means of hot air, then moistened with euca- 
lyptol or forma-percha, and a root filling of temporary stopping or 
gutta-percha packed in. If aristol be added to these the effect is 
increased. Cotton and formo-percha make a readily removable 
filling suitable to cases in wdiich some doubt exists. I have had 
excellent results in molars with this material. (See p. 551.) A tem- 
porary filling of base-plate gutta-percha is then placed in the crown 
cavity as a test filling, or, in case of need, the filling may be inserted. 

Any apical irritation may be attributed to the disinfectant and be 
treated by counterirritation, or the counterirritant may be applied 
as a precaution at the time of operation. Refrigeration of the gum 



MOIST GANGRENE OF THE PULP 579 

over the root by means of ethyl chlorid is a valuable means of reduc- 
ing inflammation in these cases. This traumatic irritation is often 
mistaken for acute septic pericementitis. Any irritation not too 
severe is to be considered as due to non-septic causes and treated 
accordingly. A few of these cases may, of course, result in failure 
owing to imperfection in the application of the method. The great 
majority of cases are successful. Still, if one desire still fewer failures, 
employ the first method. 

The withdrawal of the cotton dressing in the tentative method 
should be done under aseptic precautions. There may be found no 
collection upon cotton. In such case a fresh twist on a Swiss broach 
should be passed to the apex to determine its condition. If nothing 
be found the root may be dried and filled unless odor be present, 
when the root should be resterilized before filling, or the dressing 
renewed. 

Active hemorrhage may ensue or serum may ooze from the apical 
tissue. This may be checked with 25 per cent, pyrozone, adrenalin 
chlorid, 1 to 1000, or, preferably, alum and thymol, and the root 
filled. 

If the apical foramen be a large one, and if a pus flow follow the 
removal of the temporary dressing and be but slight, the pyrozone 
or zinc chlorid (or both) should be used and the root filled. The 
condition is one of apical abscess without fistula, and is often amen- 
able to immediate root filling. If, however, this be not considered 
advisable, the temporary dressings may be renewed, though often 
without benefit. Sometimes a thick, glairy fluid will ooze from the 
apical 'tissue. This is coagulable lymph, and the parts require 
treatment in the same manner as when a slight amount of pus is 
present. The principle involved in the departure to an immediate 
method of treatment is based upon the thorough sterilization of 
the apical tissue, the sealing of the canal to prevent infection from 
the mouth, and the prevention of effusions from the apical tissue 
into the canal. This done, the apical tissue is expected to care for 
itself. 

In order to prevent apical irritation in so far as possible, the gum 
is to be painted with ordinary tincture of iodin or spotted with the 
dental tincture of iodin, both lingually and buccally, as a counter- 
irritant. 

1$ — Iodin 3iij 

Alcohol Bj 

Shake frequently for a week or two. (Flagg.) 

If infection of the apical tissue by any chance ensue, either as the 
result of the operation of canal cleansing or previous to operative 



580 GANGRENE OF THE PULP 

interference, the disease known as septic apical pericementitis is 
established. 

Pericementitis following the opening of teeth containing gangrenous 
pulps has been explained upon the ground that the bacteria in the 
absence of free admission of oxygen have lost their virulence, which 
is restored when the air is admitted. It is quite likely that either 
this is true or that extraneous bacteria are introduced during the 
course of treatment. 

■ In case of partial moist gangrene in which a portion of a filament 
is gangrenous and the balance of it vital, or in which one root 
filament is dead and the other vital, the treatment must be varied 
to suit the requirements. The dead portion is removed as described 
and the living portions treated as ulcerated pulps. (See p. 496.) 

In a few cases the continuity of the canal has been lost because it 
has become involved in caries upon one side of the root. This may 
be treated as described on p. 432. 

Discoloration of the Teeth by Moist Gangrene. — In the final decom- 
position of the pulp a pigment molecule is formed, which, entering 
the tubules or formed in it, stains the dentin and imparts an abnormal 
color to a portion or nearly all of the crown, which ranges from 
an almost imperceptible loss of translucency to a yellow-brown, 
slate-gray, or bluish-black color. Also in conditions of venous 
hyperemia or pulpitis, with which venous hyperemia (stasis) is 
associated, the escape of the red corpuscles into the tissue, their 
disintegration, and the solution of the hemoglobin then occurs, and 
the solution enters the tubules, staining the dentin a pink color, 
which soon passes into a purplish rose, and finally becomes bluish- 
black or slate-gray. 

Those cases resulting in the yellowish or brownish coloration are 
usually associated with the loss of the pulp in comparatively sound 
or totally sound teeth, the loss occurring probably through trauma- 
tism or through slow atrophic changes, such as occur in the forma- 
tion of pulp nodules, secondary dentin, apical constriction, etc. 
Apical abscess is often much delayed, but sometimes occurs, showing 
that pulp decomposition or a later infection has occurred. The 
demonstration by Hopewell-Smith of fibrosis of the pulp and the 
obliteration of vascular structures may account for a lessened vas- 
cularity, and the absence of the production of iron sulphid because 
of the absence of necessary putrefaction and the production of the 
hematoidin products, as shown below. The first class of cases occurs 
either in sound teeth' in which the pulps have died by traumatism, 
or in filled teeth with pulps not exposed, or in teeth the pulps of which 
are exposed to the fluids of the mouth, permitting putrefactive 



BLEACHING METHODS 581 

agencies and extraneous coloring or color-setting materials to enter. 
This discoloration is most rapid in the exposed cases. 

These color changes are rationally explained by Kirk 1 as due to 
the decomposition products of hemoglobin existing in the pulp at 
the time of its death, and having an analogue in the pigmentary 
degeneration occurring in the hemoglobin in a bruise (extravasation 
of blood), in which the part becomes, first, "black and blue," then 
passes through a series of color changes, in which yellow, green, and 
bluish-black are notable. These are due to new chemical compounds 
which crystallize in the tissue. These compounds are divided into 
two classes: Hemosiderins, or those containing iron, and hema- 
toidins, those without it. Each class of these has several distinct 
substances in it, each having its own color molecule. 

Kirk states that methemoglobin is brownish-red, hemin bluish- 
black, hematin dark brown or bluish-black, and hematoidin orange. 
Jakob (Stengel) gives light pea-green and brownish-red as the 
colors of hematoidin for an old hemorrhagic focus, showing a prob- 
able slight chemical variation in the composition of the color molecule. 
As the color changes in a bruise are effected under aseptic con- 
ditions, and usually the colors finally produced are lighter than 
the "black and blue" first resulting, it is rational to suppose that 
the yellowish or brownish discoloration of teeth results under such 
conditions of aseptic decomposition (probably autolysis). These 
colors, as remarked by Kirk, are more or less permanent. 

When a permanent or progressively darkening slate-gray or 
bluish-black color is produced, it is considered by Kirk to be due to 
the formation of iron sulphid or an analogous product in which iron 
and sulphur are constituents, and that it is analogous to the black 
discoloration occurring in the visceral walls of animals undergoing 
putrefactive decomposition. The iron is liberated from the hemo- 
globin present by putrefaction, and combines with the ammonium 
sulphid which is formed from the ammonium and hydrogen sulphid 
produced by the putrefactive decomposition. 

Treatment. — The treatment of discolorations consists in what is 
known as the bleaching process, which means the reduction of the 
color molecule to another chemical molecule which is colorless, and 
then washing that out of the tubules. This is usually done by the 
use of chemicals which directly supply a molecule of nascent oxygen 
when coming in contact with the putrefactive material or its product, 
,the color molecule; or which, as chlorin, abstract hydrogen from 
the water present and so liberate a molecule of nascent oxygen, 
which combines with the color molecule. These are direct or indirect 

1 American Text-book of Operative Dentistry. 



582 GANGRENE OF THE PULP 

oxidizing agents, the effect being the same, i. e., an oxidation of the 
color molecule. A second class, as sulphurous acid, which abstract 
oxygen from the color molecule, are called reducing agents, and may 
be effective when the oxidizing agents fail. 

In the use of bleaching agents the canal should have been cleansed 
and disinfected with a simple aqueous solution of formalin or 25 per 
cent, ethereal pyrozone, or an aqueous solution of hydrogen dioxid, 
or with sodium dioxid, all oils or other materials likely to complicate 
the color molecule being avoided. With the exception of formalin, 
these are also bleaching agents and to an extent aid the subsequent 
operation. Formalin would best be avoided in cases of recent pulp 
death, as it may harden the undecomposed fibrils in the dentin. The 
upper half or two-thirds of the canal should then be filled with gutta- 
percha or oxychlorid of zinc, leaving the crown and one-third of the 
root dentin to be bleached. 

After accurate rubber damming the most valuable and facile 
method consists of placing a pellet of cotton saturated with 25 per 
cent, ethereal pyrozone in the pulp chamber and sealing it after 
careful drying of the lingual tap or cavity orifice by dropping soft, 
quick-setting cement upon the margin and sealing the entire tap. 

The rubber dam should not be removed until the cement has set, 
as the ether or oxygen gas may cause it to bulge or blister. This is 
then allowed to have twenty-four or even more hours of action, when, 
if necessary, it may be removed. The operation may be watched at 
the first or the second sitting if desired, though it may be somewhat 
prolonged. 

Aqueous 25 per cent, pyrozone may be made by shaking together 
in a test-tube one volume of distilled water and two volumes of 
25 per cent, ethereal pyrozone and evaporating the ether, the H2O2 
being left in aqueous solution; the addition of sodium acetate or 
sulphate assists the passage of the current. This is introduced by 
means of the cataphoric current, the positive pole being in the tooth, 
the negative at the hand. Occasionally the reversal of the pole 
succeeds after failure, the tubular contents probably being discharged 
with the H2O2 present in them. 

Oxygen may be liberated from sodium dioxid (Na 2 02) by sulphuric 
acid. A saturated solution of sodium dioxid is made by surrounding 
a small beaker containing about 2 drams of distilled water, with 
cracked ice. When cold the sodium dioxid powder is to be slowly 
dusted into it until it assumes a semi-opaque appearance, indicating 
saturation. In use the dried dentin is saturated with it, asbestos 
fibre being used to carry it to place, and 10 per cent, sulphuric acid is 
used to produce the liberation of oxygen with the following equation : 
Na 2 2 + H 2 S0 4 = Na 2 S0 4 + H 2 2 . 



BLEACHING METHODS 583 

The effervescence forces the tubular contents out. The sodium 
dioxid acts upon putrefactive material, decomposing it, and also 
saponifies fatty matters. 

If the operation fall short of success, this is due, in Kirk's opinion, 
to the formation of iron oxid, which can be removed with oxalic acid 
by sealing a crystal of it in the pulp chamber for twenty-four hours. 

The tubular contents being entirely removed by the sodium-dioxid 
method, the tooth is more translucent than by other bleaching 
methods in which the bleached organic debris remains in the tubules. 

The chlorin method, introduced by Truman, depends for its 
efficiency upon the affinity of chlorin for hydrogen, forming hydro- 
chloric acid (HC1) . Finding this in the water, it liberates nascent O, 
which oxidizes the color molecule, or, possibly, it abstracts H from 
the organic matter. The chlorin is usually evolved from chlorinated 
lime, that sold in paraffined paper cartons or glass bottles being the 
best. That sold in metal cans is often contaminated by the metallic 
chlorids. 

The dry powder is packed into the cavity, moistened with 50 per 
cent, acetic acid, and sealed in with oxyphosphate or temporary 
stopping for one or two days, and repeated if necessary. Only vul- 
canite, bone, ivory, or wood instruments should be used, as metal 
instruments are acted upon by the chlorin. All gold or metallic 
fillings should be removed for the same reason, and if their removal 
would cause hardship or so render the tooth into a condition indi- 
cating crowning, either this should be done or the direct oxidizing 
method tried. 

The liberation of sulphurous acid may be induced from a powder 
consisting of a mixture of sodium sulphite, 100 grains, and boric 
acid, 70 grains, separately desiccated and afterward ground together 
in a mortar, by acting upon it with a drop of water. The cavity is 
stopped by a plug of gutta-percha previously prepared and warmed. 
The following reaction occurs : 

2H 3 B0 3 + 3Na 2 S0 3 = 2Na 3 B0 3 + 3H 2 + 3S0 2 . 

In all the methods, except the use of Na 2 2 , the apex of the canals 
should be sealed before and after bleaching; at least 1 pint of hot 
distilled water should be forcibly injected into the tooth to dissolve 
out all products of chemical action remaining in the tubules, a towel 
being used to catch the drip. The tooth is then thoroughly dried, 
and if any organic matter may be present in the tubules the pulp 
cavity should be thinly lined with oxychlorid of zinc to coagulate 
it. If it has been removed, as in the sodium dioxid method, leaving 
the tubules empty, they should be filled with cavitin varnish after 



584 GANGRENE OF THE PULP 

desiccation to promote absorption, and the thin lining then placed. 
A temporary filling is to be inserted over this until success is evident, 
when the permanent work is completed with zinc phosphate and a 
metal filling. 

The removal of metallic stains has been referred to on page 335. 

Moist Gangrene of Pulps of Temporary Teeth. — The same con- 
siderations pertain to moist gangrene of the pulps of temporary 
teeth, but as the roots are resorbed to some extent or are to be 
resorbed, the root filling should be of such a character as to permit 
its resorption. Probably a combination of paraffin and aristol will 
best fulfil the indications. An iodoform paste is preferred by some. 
(See Root Canal Fillings.) 

If the roots be much resorbed, it is better to use a material which 
will permit venting of the tooth if necessary. The canals and pulp 
chamber may be filled with a combination of vaselin and aristol, and 
this covered by a filling. If trouble arise, a spear drill is driven into 
the pulp cavity from a point beneath the gum margin, establishing 
a vent. The patient should be instructed to keep this open, and be 
furnished a Swiss broach for the purpose. 

At an age when the permanent tooth will shortly thereafter erupt, 
extraction of the temporary tooth is often to be preferred to treat- 
ment. 

Root-canal Work in Cases of Gangrenous Pulps Involving Future 
Consideration. — In some cases of doubtful root sterilization or filling, 
and in which crowning by means of do welled crowns is a necessity, 
provision may be made for future relief or treatment by the employ- 
ment of one of two excellent methods of procedure : 

1 . Kirk has suggested that the post and band of a Richmond crown 
be painted while warm with a solution of gutta-percha in chloroform. 
The solvent evaporates, leaving a coating of gutta-percha. This 
should be reasonably thick. The crown is then set with cement. 
By warming the crown with a hot crown-setting tool (How) or 
forceps, it may be removed without destruction of the piece. 
Bridges so set are very firm. The crown may be set with gutta- 
percha alone or in some cases with temporary stopping. 

2. Girdwood (Edinburgh) has suggested root intubation, the tube 
being closed at the end with temporary stopping and then set with 
cement. Immediately thereafter the temporary stopping and soft 
cement are removed with Donaldson cleansers, leaving the root 
lumen free to the apical foramen or root filling. The tube and canal 
are then treated as a continuous root canal w T ould be. The idea is 
also applied to a Richmond or all-porcelain crown, the tube being 
used in place of the pin, and allowed to extend through the backing, 
to be later filled as desired. 



SECTION V. 

DISEASES OF THE PERICEMENTUM. 



CHAPTER XIX. 
SEPTIC APICAL PERICEMENTITIS (ACUTE). 

Classification — The dental periosteum and ligament, or the peri- 
cementum, is the seat of numerous nutritive and functional disturb- 
ances, which may be grouped, according to their causes, into septic 
and non-septic. 

The term pericementitis has been indiscriminately applied to all 
affections of the pericementum, and in some cases erroneously, for in 
not all affections of this structure do the phenomena of inflammation 
appear; in some hyperemia alone may exist. However, most of the 
acute and chronic degenerations are accompanied by evidences of 
inflammation. 

Bodecker's division of the affections of the pericementum into 
purulent and non-purulent is misleading. Cases may be due to 
septic causes without pus formation; pus formation represents but 
one form of sepsis. 

The most convenient clinical classification of these disorders is that 
offered by G. V. Black: 1 (1) Diseases of the pericementum beginning 
at the apex of the root; (2) those beginning at the gum margin; (3) 
those beginning in some intermediate portion of the pericementum. 
These may again be divided, according to their causes, into septic 
and non-septic. Another clinical classification would be into localized 
and general disturbances — another into acute and chronic. 

Evidences of Pericemental Disturbance — It was noted in the 
study of the diseases of the dental pulp that the diagnostic signs of 
pulp disturbance were exaggerated or diminished response to thermal 
stimuli; reflected instead of localized pains; and, except in rare cases 
of advanced hyperemia, no tenderness upon percussion. Disturb- 
ances of the pericementum are accompanied by entirely different 
symptoms which serve to distinguish between them and diseases of 

1 American System of Dentistry, vol. i. 

(585) 



586 SEPTIC APICAL PERICEMENTITIS 

the pulp. They are, in general, tenderness upon percussion. As 
shown by Black, 1 the pericementum is the touch organ of the tooth, 
its tactile organ, through which a tooth locates force applied to the 
tooth. The pains of pericemental disturbance are, therefore, in the 
majority of cases, exactly localized, instead of not being localized, 
as in the case of the pulp. A tooth tender upon percussion has 
its pericementum as the seat of disturbance. Most cases of peri- 
cemental diseases are accompanied by vascular reactions ranging 
from an increased blood flow, or grades of hyperemia to pronounced 
inflammation, and have the corresponding symptoms. The increased 
volume of the pericementum causes the protrusion and loosening of 
the tooth, heightened sensitivity being the accompaniment. As the 
vascular supply of the pericementum and that of the gum are in a 
degree collateral (see p. 190), evidences of vascular engorgement 
are seen in the gum overlying the affected tooth. Owing to the 
altered density of the parts surrounding the tooth root, percussion 
upon the tooth elicits a different sound from that observed in health 
— the sound is dull. The general symptoms of pericemental affections 
are, therefore, tenderness upon percussion and a dull percussion note, 
more or less protrusion, and looseness of the tooth and a deepening 
of the local gum color. 

DISEASE OF THE PERICEMENTUM BEGINNING AT THE APEX. 

Diseases of the pericementum beginning at the apex of the root 
are of two classes, septic and non-septic. The septic cases are almost 
invariably the sequel to diseases of the pulp, namely, suppuration 
and gangrene, or arise in consequence of infection through the canals 
of pulpless teeth. The non-septic cases are due to mechanical and 
chemical irritants, and in rare cases to undiscovered causes. 

Acute Septic Apical Pericementitis ; Acute Alveolodental Abscess ; 
Dento-alveolar Abscess. — Definition. — By septic apical pericementitis 
is meant an inflammation of the apical pericementum due to the 
entrance of bacteria into the tissue lying in the apical space. 

Causes. — The most common causes of septic apical pericementitis 
are : 

1. Bacteria engaged in the putrefaction of a gangrenous pulp. 
The gases and toxic products evolved by the process also cause 
much irritation. 

2. Pyogenic organisms engaged in the production of suppuration 
of the pulp in its later stages. 

1 American System of Dentistry, vol. i. 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 587 

3. Pyogenic organisms introduced into the otherwise aseptic tissues 
of the apical space by means of instrumentation or other lack of 
aseptic precautions. 

Fig. 534 




Alveolar abscess pointing externally. The abscess is caused by the only-slightly- 
impacted and not-malposed lower, third molar. (Raper). 



4. Infection of an apical space by an abscess arising in some con- 
tiguous part and extending in the direction of the apical space under 
consideration. 

5. Septic infection from a pyorrhea pocket located upon the side 
of the tooth in question, the deepest portion of which approximates 



588 SEPTIC APICAL PERICEMENTITIS 

the apical space. An alveolar abscess about an impacted tooth 
may find its way apically and even discharge through the cheek. 

6. Possible infection by way of the pericemental tract from the 
gum margin or by way of the circulation, which infection may cause 
a pericemental abscess located in the apical tissue. 

The last two conditions would be septic apical pericementitis, 
but are to be considered separately as pericemental abscess or true 
alveolar abscess. (See Pyorrhea Alveolaris.) As a cause of apical 
abscess it is rare, but has been seen. 

Apart from these causes infective inflammation of apical tissue 
does not seem to occur. It is to be remembered that a small portion 
of gangrenous pulp beneath a root-canal filling is equivalent to an 
entire gangrenous pulp as a cause of pericementitis. The vast 
majority of cases occur as a sequel to moist gangrene of the pulp, 
either before or after instrumentation, or as a result of infection of 
the apical tissue by instruments either unsterilized or reinfected by 
contact with the oral fluids. 

The organisms found in acute apical abscesses are those usually 
found in gangrenous and suppurating pulps, and in a certain per- 
centage of even healthy mouths. (See p. 51.) Schreier found the 
Diplococcus pneumoniae in 15 out of 20 cases examined. He also 
found Staphylococcus pyogenes albus and aureus, and occasionally 
Streptococcus pyogenes. 

Arkovy found the Bacillus gangrense pulpse in a number of cases. 
(See p. 568.) These are virtually the same organisms that are found 
in the deeper portions of a suppurating or gangrenous pulp; this 
fact in itself is enough to show the continuity of infection from the 
pulp canal. It is a well-known clinical fact that acute outbreaks of 
septic apical pericementitis are most liable to occur under those 
conditions when patients "take cold." Schreier points out that 
these atmospheric states produce a bodily condition which favors 
the development of the Diplococcus pneumoniae (Pneumococcus), 
and finds in the association of these factors the reason why this 
diplococcus should be pathogenic in the dental condition. 

Pathology, Morbid Anatomy, and Symptoms. — The Inflammatory 
Stage. — As in abscess elsewhere there is first infection by pyogenic 
organisms which produce the phenomena of infective inflammation 
within the substance of the apical tissue, and in the later stages in 
the contiguous tissues. 

Following the infection, arterial hyperemia is produced, sensation 
is exalted, and the tooth becomes tender upon percussion; but if 
forcibly pressed upon — i. e., if the arteries be compressed — the 
hyperemia is momentarily lessened and the pressure brings a sense 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 589 

of relief. At this stage the gum over the apex looks normal, but 
may respond to pressure. 

Following the arterial hyperemia, the venous obstruction which 
ends in stasis is inaugurated and diapedesis of leukocytes and fibrin- 
ous exudation into the intervascular tissue occurs. The fixed cells 
undergo proliferation. 

Fig. 535 




Showing the morbid anatomy of septic apical pericementitis (acute): A, pus; B, 
area of dying leukocytes; C, septic matter in root canal; D, inflammation of process 
(osteomyelitis; area of lesser inflammation); E, swollen periosteum and gum, hyper- 
emic; F, alveolar bone in a stage of hyperemia; G, pericementum at edge of necrosis. 



As this condition of inflammation becomes established the pain due 
to pressure upon the sensory nerves becomes of a violent throbbing 
character, accompanied by a sense of fulness. The swelling of the 
tissue about the apex of the root, due to the excess of fluid, blood, 
leukocytes, and tissue cells, of necessity pushes the tooth from its 
socket, so that it feels and is longer than the other teeth. Moreover, 
as it is bitten upon the apical tissue is further irritated. The tooth is 
loosened and percussion induces pain and elicits the dull note which 
is diagnostic of the increase of bulk in the pericementum. The color 
of the gum over the root becomes deepened. 

First Stage of Pus Formation. — The central area of the apical 
tissue — i. e., that next the apical foramen — is broken down into pus, 
some of which enters the root canal (Fig. 535, A). As the area of 
pus formation widens, all of the apical tissue is liquefied (Fig. 538, a). 



590 



SEPTIC APICAL PERICEMENTITIS 



From a clinical point of view the abscess is incipient when inflamma- 
tion of the apical tissue next to the foramen is profound, and pus 



Fig. 536 



Fig. 537 





A cyst extending from left lower second bicuspid to 
the central of same side. The central has a root filling. 
Method of accurately de- In absence of other things this may be regarded as the 
termining length of root. origin of the cyst. 



Fig. 538 




Acute abscess in second stage. Tooth opened at b for treatment, making an abscess, 
discharging via the canal. (Black.) 



Fig. 539 



Fig. 540 







Abscess on crowned root. (Skiagraph 
by Lodge.) 



Abscess on incomplete root. (Skia- 
graph by Lodge.) 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 591 



Fig. 541 



formation has just begun (Fig. 535). The first stage continues while 
the pus is in the apical tissue. 

Second Stage of Pus Formation. — The bone cells become 
involved in the process and are destroyed (osteitis). The throbbing 
pain, the extrusion, looseness, and dulness to percussion, and the 
inflammation and edema of the contiguous tissues are marked. The 
gum is widely inflamed, reddened, and swollen, but no demarcation 
of an abscess may be noted upon the gum at this stage. The mem- 
branes of the adjoining teeth become irritated and hyperemic, and 
they may exhibit tenderness upon percussion (Fig. 538). 

Third Stage of Pus Formation. — The pus continues to form 
in all directions until the bone is perforated at some point — i. e., 
usually through the labial alveolar plate — that being the thin- 
nest and most readily per- 
forated. The periosteum is 
now destroyed and the gum 
tissue directly involved as a 
boundary to the pus, which 
collecting beneath it, raises it 
into a distinctly demarked 
tumefaction (Fig. 541, b). The 
pain becomes less acute, ow T ing 
to the binding resistance of 
the gum being less than that 
of the bone. At first the 
swelling .is hard, and this 
represents a mass of gum tis- 
sue overlying pus; later, it 
softens at its highest point, 
pus appears as a yellow spot 
beneath the mucous mem- 
brane. The mucous mem- 
brane bursts and a discharge 
of pus follows. The inflam- 
mation and tenderness then 
largely subside, but some de- 
gree of looseness and protru- 
sion remains. 

During the latter part of the second and in the third stage of pus 
formation, instead of the swelling extending but little beyond the 
overlying gum, the tissues of the lips, cheeks, or neck may be very 
much swollen and with upper teeth the eye of the affected side 
injected. In some cases the outer skin may become reddened and 




Acute alveolar abscess of a lower incisor in 
the third stage, with pus cavity between the 
bone and the periosteum: a, pus cavity in 
the bone; b, pus between the periosteum and 
bone; c, lip; d, tooth; e, tongue. (Black.) 



592 SEPTIC APICAL PERICEMENTITIS 

dusky, exhibiting the evidences of extension of the inflammatory 
process far from its original site. 

The inflammatory process spreads out from the central focus of 
pus formation, there being around the pus a zone of active inflamma- 
tion or stasis; about this one of a lesser degree of inflammation, also 
full of leukocytes; about this an area of arterial hyperemia or the 
first stage of inflammation, and around this normal tissue. These 
areas are not sharply defined, but merge into one another (Fig. 535, 
A, D, E, F; also p. 135 and Fig. 64). 

In this way the contiguous area of the alveolar bone and the soft 
tissues of the face become involved in the process, being discolored 
and tumefied in proportion to the extent of the pus formation and 
the inflammatory reaction thereto. 

While in the vast majority of cases the direction taken by the pus, 
and the point at which it finds exit, is the buccal or labial aspect, and 
immediately over the root apex of the affected tooth, or near it, 
these being the directions of least resistance, other anatomical con- 
ditions or histological peculiarities may make the direction of least 
resistance in some other path (Figs. 542 to 545). 

Instead of the circumscribed suppuration described as the ordinary 
course of abscess formation about the apices of roots (septic apical 
pericementitis) which accompanies infection by the staphylococci, 
clinical evidences of infection by streptococci occasionally appear. 
The inflammatory process, instead of being circumscribed, is diffuse; 
the inflammation extends along the lines of the connective tissues 
and of the lymphatics; the connective tissues are swollen, the swelling 
extending to the tissues of the cheek, down the neck, and even to 
the shoulder — a phlegmonous inflammation. Instead of the com- 
paratively free flow of pus which follows incision of the swelling in 
ordinary abscess, pus formation in streptococcus infection is seen, 
upon incision, to be limited and seropurulent. While in alveolar 
abscess of the ordinary types evidences of septic intoxication or 
poisoning are unusual, the lymphatics being blocked, as a rule, by 
the inflammatory exudates, septic intoxication and poisoning are the 
rule in the erysipelatous cases, those probably due to streptococcus 
infection; bacterial poisons being taken up by the lymphatics find 
their way into the circulation. 

The symptoms of the absorption of bacterial products from the 
circumscribed abscesses are: Fever, often ushered in by a distinct 
chill. The pulse increases in volume and tension; it is full, hard, 
and frequent. The tongue is coated, the bowels constipated. The 
patient is also weakened and made irritable by pain and attendant 
loss of sleep and appetite. 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 593 

In the streptococcal infection there is danger that these may 
change into the more profound symptoms of septicemia — i. e., a 
soft, frequent pulse, repeated chills, diarrhea, clammy skin, general 
depression, and a disordered nervous system. 

In multirooted teeth the inflammation and abscess frequently 
appear on only one root. If the case be seen early, before the active 
exudation period of the inflammation sets in, the symptoms may be 
clearly localized in one root, the tooth exhibiting tenderness upon 
pressure over the affected root, but not upon the opposite side. 

After spontaneous discharge of the pus from an abscess, the 
condition remaining is that of an ulcerous surface (the abscess 
boundaries) which is being continuously infected from the putrescent 
pulp remnants. The conditions, it is seen, are not like those of 
ordinary abscess, where the infective material is largely discharged 
in the pus evacuation, and the cells bounding the abscess wall 
dispose of remaining bacteria, so that regeneration of tissue occurs. 
Spontaneous healing of an apical abscess is the exception; the 
embryonic tissue lining the abscess walls, being continuously infected, 
degenerates and dies as fast as it forms, leaving a condition known 
as chronic apical abscess, or chronic purulent, apical, septic peri- 
cementitis. 

Clinical History. — The clinical history of acute alveolar abscess 
may be divided into three stages: (1) That of initial inflammation 
and pus formation: (2) the destruction of the alveolar process; (3) 
the passage of pus through the periosteum and mucous membrane. 
The second stage is usually the longest. The duration of the disease 
depends upon the readiness with which the tissues between the point 
of beginning pus formation and its exit yield. When the pulp 
chamber is open pus may find exit by this path, constituting the 
condition known as blind abscess — a misnomer, because a blind 
abscess is one without a point of discharge, without a fistula leading 
to it; in the cases discharging via the canal, the latter may be 
considered a fistula (Fig. 538). 

Acute abscesses usually run a short course, the inflammatory 
symptoms being severe and the tissue destruction limited. Notably 
upon lower molars, and upon the lingual roots of upper molars, 
the density and thickness of bone overlying the roots may make 
paths of greatly increased resistance, so that the destruction of 
tissue proceeds along the line of the pericementum, the pus finding 
exit at the neck of the tooth. It is rare in cases of lower second 
molars, and still more rare upon the third molars, that pus finds 
exit over the apex of the root, the dense bone of the external oblique 
line offering the greatest resistance (Fig. 542). Over any teeth 
38 



594 



SEPTIC APICAL PERICEMENTITIS 



the outer fibrous layers of the external periosteum may present 
unusual resistance to the perforative advance of pus, so that when 
the fibers of attachment of the periosteum have been softened by 
the inflammation, and pus gains entrance between bone and peri- 
osteum, it may travel or burrow along the course of this membrane 
(Fig. 543), depriving the bone of its main nutritive source, so that 
limited necrosis threatens. The roots of the central incisors may lie 
unusually close to the floor of the nose, and be overlaid externally 
by an unusually resistant layer of bone; in these cases the path of 
least resistance may be in the direction of the floor of the nose, the 
abscess opening at that point (Fig. 544), or the pus may perforate 
the lingual alveolar plate, and, raising the periosteum and mucous 
membrane, form a large swelling upon one side of the hard palate. 



Fig. 542 



Fig. 543 





Abscess upon lower third molar, 
showing the usual paths of pus exit, A 
and B. 



Abscess upon palatal root of an upper molar 
discharging at the neck of the tooth. 



Vederspiel 1 instances a case in which an abscess starting upon 
an upper third molar finally infected the tonsil producing an abscess, 
also produced necrosis of a portion of the ramus of the inferior 
maxilla. 

The root apices of the posterior upper teeth, particularly of the 
first and second molars, may, after the age of twenty-five or thirty, 
be encroached upon by the enlarging maxillary sinus, so that any 
or all of the roots of these teeth may be separated from the floor of 
the sinus by but a very thin lamina of bone or only by periosteum 
and mucosa; should abscess arise upon any of these roots, pus 
discharge into the antrum would necessarily follow. In these cases 
the acute symptoms may rapidly subside, but later symptoms of 
antral empyema may follow (Fig. 545). 



1 Dental Cosmos, December, 1912. 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 595 

Resort to the use of poultices upon the face, for the relief of the 
pain of abscess formation, may induce such a softening of the tissue 
over which they are applied that the passage of pus is invited toward 
the exterior; the abscess may thus open upon the face or neck, 
producing permanent, disfiguring scars (Fig. 583): 



Fig 544 



Fig. 545 




Alveolar abscess at the root of a 
superior incisor, discharging into 
the nose: a, large abscess cavity in 
the bone; b, mouth of fistula on 
the floor of nostril; c, lip; d. tooth. 
(Black.) 




Alveolar abscess at the root of an upper 
molar discharging into the antrum of High- 
more: a, abscess cavity in the bone; b, 
mouth of fistula on the floor of the antrum ; 
c, pus in. the antral cavity. (Black.) 



In patients who are in a cachectic condition, who have an evil 
heredity, or whose tissue resistance is markedly lessened in conse- 
quence of tuberculosis, or more frequently of syphilis, septic peri- 
cementitis may run a riotous course; the bone suffers extensively by 
direct action; the periosteum is undermined, is stripped from the 
bone over large areas, and breaks down readily; so that while in 
the healthy person alveolar abscess formation may run a direct 
course and find prompt outlet, in the syphilitic patient extensive 
pus infiltration, with necrosis, may occur. In cachectic persons lym- 
phatic involvement is common; waste products of bacterial origin 
find their way into the lymphatics, and set up secondary irritative 
processes in the nearest lymphatic glands — lymphadenitis. 

In persons w T hose oral hygiene is neglected the third stage of 
alveolar abscess is frequently violent and the inflammatory process 
widespread. 

Diagnosis. — In incipient apical pericementitis the symptoms may 
consist of reflex pains, but, as a rule, are distinctly localized in the 
teeth affected, which are tender to the touch. The discoloration of 
the tooth crown and other evidences of moist gangrene are usually 
present unless the tooth has been previously partially treated, when 



596 



SEPTIC APICAL PERICEMENTITIS 



the color may be good, but by transmitted light opacity is noted 
In a few cases the tooth has had almost a normal color even under 
the transmitted light. In the pronounced cases the symptoms are as 
described (see p. 570). 

When a sinus is present a soft silver probe may often be passed 
toward the tooth affected. 

A timid patient will often unintentionally confuse pericemental 
tenderness with the pain of sensitive dentin. 



Fig. 546 



Fig. 547 





Diagnosis of apical abscess by- 
x-rays. (Price. 1 ) 



Skiagraph of perforation and apical abscess; wire 
thrust through same. (Lodge's method.) 



In very doubtful cases, as when molars have deep amalgam fillings, 
or pins have been placed in root canals, or gold crowns cover the 
natural crowns, either the covering must be removed or a skiagraph 
be taken. 

After high inflammation has existed for twenty-four hours, pus is 
generally present in the apical tissue. 

Of two pulpless teeth surrounded by a zone of inflammation, the 
more tender and loosened is the one affected, though both may be 
acting at once. It is to be remembered that adjoining, otherwise 
normal, teeth may show some evidence of pericementitis, due to 
extension, so that differentiation is necessary. The various stages 
of inflammation and pus formation are judged by the appearance of 
the gum or by the arrays (Fig. 546). The greater the swelling and 
injection of the gum, the more advanced is the pus formation. 

The inflammatory action precedes the advance of pus, which 
furnishes a guide to the direction the pus is pursuing — viz., where 
the most intense coloration and the greatest swelling appears will be 
the point at which the abscess will point or discharge. A sudden 
subsidence of inflammation without an immediately discoverable 



Items of Interest, 1901. 



Fig. 548 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 597 

point of pus exit should lead to the suspicion that the discharge has 
taken place in an unusual situation. 

The direction pus may take is often determined by gravity, but 
the resistance of certain tissues may cause the pus to seek the easiest 
path. Thus, by discharging into the antrum it goes rather counter 
to gravity. In such cases as discharge into the antrum there is 
liable to be a collection of pus in that cavity which may cause destruc- 
tion of the mucous membrane and bone. This condition is known 
as empyema of the antrum. The 
sudden subsidence of an acute abscess 
upon a tooth located beneath the 
antrum should create a suspicion of 
discharge into that sinus. If a fine 
probe can be passed an unusual length 
into a root canal it indicates this form 
of sinus involvement. 

An abscess originating about an im- 
pacted tooth, or one due to subperio- 
steal inflammation, must be differen- 
tiated 1 (Fig. 548). A pericemental 
abscess must also be considered. It is 
always more lateral and there is less 
facial involvement, also there is usually 
a pyorrhea pocket leading to it. An 
acute abscess of the pulp in its most 
pronounced stage may simulate incip- 
ient or- even pronounced acute apical pericementitis. (See p. 449.) 
An abscess sometimes forms beneath the flap of gum overlying a 
third molar. This begins as an ulceration of the under side of the 
flap, but the pus burrows between the tooth and the gum, and when 
well confined may develop laterally, causing the formation and at 
least partial retention of a quantity of pus in the tissues of the cheek. 
This condition more nearly simulates the lateral abscess associated 
with a pyorrhea pocket, and as by extension it sometimes involves 
the tonsil, the case may be mistaken for an amygdalitis. 

The last three conditions are usually associated with suspected 
teeth containing vital pulps, so that tests for pulp vitality are to be 
applied. 

In certain cases of pulp gangrene part of the pulp only may be 
dead — e. g., the lingual filament of the pulp of an upper molar; while 
the balance may be vital (the buccal filaments) . This fact may con- 




Non-descended cuspid and lat- 
eral. These teeth were entirely 
enveloped in pus. The cuspid 
and lateral shadows overlie each 
other. Between these and the 
first bicuspid may be seen three 
tiny supernumeraries. (Lodge.) 



1 Black: American System of Dentistry, vol. i. 



598 SEPTIC APICAL PERICEMENTITIS 

fuse the response to tests and is to be borne in mind. A broken root 
covered more or less by gum or carious bone must be taken into 
account. 

Prognosis. — In the majority of cases the prognosis of acute apical 
abscess, as to the future retention of the tooth, is favorable; and 
usually very favorable if the case receive intelligent therapeutic aid. 
The future of the tooth depends upon the thoroughness with which 
sources of infection may be destroyed and permanently removed, 
and the completeness with which regeneration of tissue can be induced. 

Treatment. — In the initial inflammation and first stage of pus for- 
mation the treatment should be abortive, to afford relief from the 
pain. The cause of the inflammation should be removed, if possible, 
and the pus formed be removed or, at least, permitted to escape by 
way of the pulp canals. The promptness of relief from pain depends 
upon the thoroughness with which this is accomplished. 

The pulp chamber should be opened to an extent which permits 
the free passage of broaches into the canal (Figs. 538 and 543). 

If the cavity of decay be open, the pulpal wall is to be perforated. 
If a filling be present, it is in part or entirely removed. If the enamel 
be entirely sound, or if subsequent treatment require a new opening 
in line with the pulp canals, it is at least in part made. 

These openings are usually begun with a small, spear-pointed drill 
(No. 100, S. S. W. Catalog) revolving in a perfectly true hand piece. 
To centre the drill, first spot the enamel with a dentate bur. The 
opening made is enlarged with successive sizes of sharp, round, 
dentate burs until of sufficient size. 

According to the amount of tenderness, the tooth will require a 
count erpressure to that of the drill. If the entrance be made through 
the occlusal face of the tooth, or in a direction which would cause 
direct pressure on the apical pericementum, a ligature of linen 
thread with long ends may be placed around the tooth, and traction 
be made by drawing on the loose ends of the ligature. 1 Effective 
counterpressure against lateral entrance to the pulp chamber may 
be made by softening a small roll of modelling compound and mould- 
ing over the face of the affected tooth and several of those adjoining 
it, and hardening with cold water. This temporary splint is held in 
place by the index finger of the left hand. W. D. Tracy recommends 
for posterior teeth a double modeling compound splint, one lingual 
one buccal, to be held with the fingers, or two ligatures may be 
placed between the tongue before the compound is placed and the 
ends tied over the splints, binding them against the teeth. In case 

1 J. Foster Flagg: Lectures on Dental Therapeutics. 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 599 

the inflammatory process is marked, or if the patient be in bed, it 
may be necessary to make a vent opening by the easiest path, espe- 
cially when using a hand drill — i. e., at the junction of enamel and 
cementum — directly into the chamber. 

As soon as entrance to the pulp chamber is effected, the cavity 
is syringed with a strong antiseptic. Fine probes are passed and 
repassed into the opening to free the outlet, so that gases and pus 
may escape and fresh portions of the antiseptic be worked into the 
cavity. The escape of blood from the canal is a sign that all the pus 
is vented. The quickness with which relief is secured will depend 
upon the thoroughness with which the canals are entered and their 
putrid contents given vent. A tedious class of cases are those in 
which a canal of a molar is filled or partially filled. Unless entrance 
to and cleansing of the canal be accomplished, the inflammation 
will proceed until the pus finds external vent. An hour spent in 
gaining access to and cleansing such canals is well spent. 

The patient may be directed to make suction with the tongue 
to create a vacuum tending to draw the pus, etc., into the canal. 
If a tight joint can be obtained with a special point an abscess syringe 
may have its plunger drawn back to create the vacuum. This 
measure is not necessary when prompt relief is obtained by venting. 

The canals may be dried and an anodyne antiseptic, such as 
phenol camphor plus menthol, pumped into them. If, now, pro- 
vision against mastication upon the elongated tooth be made by 
means of a guard, relief is tolerably certain. 

Watkins 1 has used "blue light" applied from a 16-candle power 
blue-globed electric lamp through a funnel directly upon the part. 
He claims relief from the pain, enabling him to open the tooth 
previously too painful to be operated upon. He also claims that 
swelling is much reduced by it, in some cases in twenty minutes. 
The high frequency current is also useful in this connection. 

Patients do not ordinarily tolerate the rubber dam in these cases, 
and as the tooth should be left open it need not be used. 

A guard may be made from a strip of rubber dam two inches long 
and of a width corresponding to the distance from the buccal to the 
lingual gum margins and folded into a pad of the width of the 
occlusal face of the tooth to be covered. Floss silk is then sewed 
through this in such a manner as to cause it to tie the pad over the 
tooth, the silk itself encircling the neck of the tooth. 2 This should 
fce attached to a nearby tooth, and will insure rest of the affected 
pericementum by preventing occlusion upon the crown (Fig. 549). 

1 Dental Cosmos, 1905. 2 Flagg. 



600 SEPTIC APICAL PERICEMENTITIS 

Cold antiphlogistics, such as lead water and laudanum or cata- 
plasma kaolini, should be applied externally. No hot external 
applications should be used in abscess cases, as they may cause an 
external fistula to be formed. 

The mouth is to be frequently washed with an antiseptic. In 
simple cases with prompt relief this is all that is necessary; in marked 
cases the reduction of the inflammatory engorgement should be 
attempted in addition. 

Swedish leeches may be applied to the gum, or a cut or two made 
in the gum over the apex of the tooth will allow free bloodletting 
and drainage of the excess of blood in the pericementum. A hot pedi- 
luvium and a saline cathartic conjoined are useful as counterirritant 
derivatives, and the latter is also depletive, reducing the volume of 
the blood. The hot pediluvium with mustard added and diaphoresis 
conjoined are also useful. Ten grains of Dover's powder in divided 
doses in hot lemonade are given, in part, while the pediluvium is 
being administered, and the patient is later well covered up in bed. 

Fig. 549 



rr 




Rubber dam guard for use in pericementitis: A, roll of dam threaded; B, guard fitted 
over tooth ; tooth eliminated to show the manner in which the silk encircles it. 

Quinin in doses of gr. vj is given as a febrifuge and to limit exu- 
dation, and tincture of aconite, two drops at first, and one-half drop 
each half hour is given until the volume, tension, and frequency of 
the pulse are reduced. 

If syphilis be a complication in these cases, potassium iodid, in 
doses of 10 grains each three hours, is useful as an antagonist of its 
influence and as a nervous sedative. Unless Dover's powder is used, 
morphin sulphate in blondes and morphin bimeconate in brunettes 
(especially those with blue eyes), or any persons with known idio- 
syncrasies to morphin, should be administered in f grain doses, 
repeated each hour up to f grain. When great suffering renders it 
necessary, a hypodermic may take its place. When used, a saline 
cathartic should be given the following morning. Trigemin is useful. 

These several measures are to be regarded as the abortive treat- 
ment of alveolar abscess; they apply to all cases if seen early enough, 
and will in the majority of cases prevent the disease of the peri- 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 601 

cementum passing the early inflammatory stages. In all cases the 
severity of the inflammatory process is lessened in proportion to 
the thoroughness with which the antiseptic measures are applied, 
provided that in the attempt at such application no septic matter 
be violently thrust through the apical foramen, especially of the one 
of a multirooted tooth which is not involved. 

The Second Stage of Acute Apical Abscess. — In very mild stages the 
pus is in the bone and the infection considered more virulent, i. e., 
the germs are specially active. The abortive treatment should first 
be tried, and if free venting of pus is obtained relief is usually given. 
If not given the case continues to the third stage. If bearable, or 
the surgical method be impracticable, a dental capsicum plaster 
may be applied to the gum or a roasted half-raisin may be applied. 
Either causes an inflammation of the gum, which advances the tissue 
that much nearer suppuration. Thus it prepares a readily invaded 
tissue and hastens pointing. The contrary effect has sometimes 
been produced, and is explained upon the ground that the increased 
amount of blood has increased the phagocytosis and destruction of 
bacteria or has stimulated a restoration of the circulation, possibly 
both. Trigemin is a useful adjunct when the pain is severe. For 
the purpose of hastening suppuration, calx sulphurata, J grain each 
hour, is useful. It also sometimes hastens resolution. It is proper 
to denominate this the expectant treatment, and while, perhaps, 
unsurgical, at times permits no alternative except extraction. 

When tolerable or imperative, the surgical method of venting the 
abscess through an opening in the gum is valuable. The apical 
region- is located as nearly as possible by measuring the length of the 
tooth with a probe passed into the canal and over which a small 
piece of rubber dam is slipped as a guide. This is laid over the 
crown and gum and a tiny drop of carbolic acid is placed just above 
the point of the probe as a guide. A vertical cut is made in the 
gum down to the bone, and a broad spear drill is driven through it 
into the abscess tract. Whether this shall be done under ethyl 
chlorid refrigeration, local anesthesia, or short general anesthesia, the 
operator must determine. 

A gradual perforation is useful in some cases. This method, 
designed by Black, consists in gradually escharing and scratching 
the gum tissue. Successive applications of just such carbolic acid 
as adheres to the point only of a sharply serrated plugger are made, 
.followed by slight scratching only so that blood shall not be drawn. 
In this way the bone is ultimately reached. 

A fresh drop of acid is applied, the periosteum scraped away 
slightly, and the drill then used. 



602 



SEPTIC APICAL PERICEMENTITIS 



A Rollins tubular knife (Fig. 550) has been used with success to 
remove a piece of gum, after which the drill or a fine trephine 
(Fig. 551) is used. Some acute pain may follow this operation, but 
usually lasts only a short time. 



Tubular knives. 



Walker- Younger trephines. 



If antiseptics are used to syringe out the abscess cavity, it is better 
to use a mixture of six parts hamamelis (aqueous) and one part 
listerine as a partial sedative. , The use of hydrogen dioxid is often 
very painful, owing to the rapid reaction with the blood present, and 
as it sometimes also drives the infective material into remote parts 
without disinfecting it, its use in this connection is not without 
danger, and should be avoided. 

It has been a subject of controversy whether a tooth should be 
extracted while the abscess is in the second stage. It has been 
claimed that the continuation of pus formation after extraction 
renders the state of the patient worse than before extracted. 

This occurrence is comparatively infrequently seen, and is, of 
course, due either to the retention of some pyogenic organisms 
beneath the clot which forms in the alveolus or the infection of the 
parts by extraneous organisms. 

The retention of the tooth until a fistula forms would also confine 
the bacteria for the time. 

Unquestionably metastatic infections have appeared as the result 
of persistent local infection following tooth extraction, the avenue 
being the lymphatics; therefore, in cases of extraction during the 
second stage of pus formation the alveolus should be forcibly syringed 
for ten minutes with the above listerine solution. If it be thought 
desirable to repeat the syringing, a tent of antiseptic gauze may 
be gently carried to the apex of the alveolus and left. This tent 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 603 

may be removed to permit syringing, and should never be left long 
at any one time, as septic inflammation of the alveolar walls may occur. 
It also does not drain pus readily, so it might cause an abscess if 
left too long. 

In cases of this kind oral sterilization and anti-infective systemic 
medication are of importance. As soon as improvement is noted the 
tent should be removed, the alveolus sterilized as before, and a new 
clot induced by a curetting of the walls. The case should now pro- 
ceed as any ordinary extraction; if not, it should be treated as for 
dry socket (which see). 

In a reply to a circular letter of questions regarding this point, 
Black, Kirk, Ottolengui, HorTheinz, and Schamburg all favored 
extraction as a means of removal of the cause and as a less evil than 
allowing the tooth to remain enclosing the bacteria, which, if cap- 
able of producing septicemia, it would do if allowed to remain. They 
are therefore in agreement with the editor's position taken in the 
second edition of this work (1904). Brown argues the difficulty of 
decision in an individual case. All are practically opposed to the 
idea that pneumonia is more likely to result from postextraction 
sepsis than septicemia, Morris 1 having taken the position that 
pneumonia resulted from extractions in this condition. Each and 
all advised careful ante- and postextraction antisepsis. 

The editor has had quite a number of cases of necrosis (necrotic 
dry socket) following extractions at the hands of specialists, and 
believes they and he should have been more watchful in these cases, 
and that in most cases a strong solution of potassium permanganate 
should- be used as a wash before and after extraction, or tincture 
of iodin be locally applied, especially in cases requiring laceration 
of the gum. Antiseptic spraying of the alveolus, etc., is a reliable 
measure. In one case of extraction of a lower third molar opera- 
tion under anesthesia for prevention of progressive necrosis became 
necessary. The making of a cautious diagnosis and awaiting the 
proper time, as recommended by Mitchell, is a physical impossi- 
bility unless one await the third stage or a fistula or general infection, 
as in this state the bacteria are considered virulent, especially while 
bone solution is in progress. 

The Third Stage of Acute Apical Abscess. 1 — In this stage the pus 
has found its way through or beneath the periosteum on the outside 
of the bone; therefore its germs are engaged in liquefying the gum 
tissue or in unusual location the mucosa or muscular tissue of the 
part. Except in these cases the gum is tumefied, a hard, circum- 

1 Mitchell: Dental Cosmos, 1907, p. 713. 



604 SEPTIC APICAL PERICEMENTITIS 

scribed, inflamed nodule indicating pus near the bone, a soft, more 
generally diffused swelling indicating more superficially located pus, 
while a soft yellow or yellowish-pink tumefaction indicates pointing. 
In all these cases the indication is for a surgical opening of the gum 
rather than the opening of the tooth. The part should be gently 
disinfected with tincture of iodin on a ball of cotton, and a sharp 
bistoury should be boldly driven to the bone, with the cutting edge 
turned toward the occlusal. The lip or cheek is to be drawn well 
away to avoid injuring the coronoid, buccal, or facial artery. A cut 
about a half to three-quarters of an inch in length is rapidly made by 
sweeping the edge and point downward occlusally. Too deep lancing 
upon the hard palate may injure the posterior palatine artery. 

As this is usually painful, it is better to refrigerate the gum with 
ethyl chlorid or operate under short general anesthesia, e. g., nitrous 
oxid or the first impression of ether. Novocain is only useful in the 
case of deep-seated pus injected into the more healthy tissue. Next, 
the abscess tract is to be gently washed out with a diluted hama- 
melis solution, preferably warmed. Fairly hot water containing an 
antiseptic also gives relief. 

If the abscess has been deep-seated it is well to introduce a fine 
tent of antiseptic gauze through the opening into the abscess tract 
to prevent the too rapid healing of the external orifice which is apt 
to occur, owing to the approximation of the lips of the wound pro- 
duced by cheek pressure. This healing sometimes permits a second 
collection of pus. The tent should be removed not later than the 
next day, the abscess tract disinfected again, possibly with a mer- 
curic chlorid solution, and the tent replaced. At this time the tooth 
should be opened and disinfected if not tolerable at the first sitting. 
When this is tolerable the crown may be tapped and formocresol 
sealed in the pulp chamber, just before the operation of lancing, in 
order to permit disinfection and thus limit pus formation and to save 
time. Tents in aveoli should never be left long at a time, as they 
become septic and may cause necrotic conditions of the alveolus. 

The patient should always be cautioned to remove the tent if 
swelling return, as this indicates a stoppage of the vent, with collec- 
tion of pus. 

When diffuse cellulitis with marked febrile disturbance passing 
into the adynamic type is produced, one should fear the infection 
with Streptococcus pyogenes and treat not only locally, but use 
blood germicides against a possible septicemia. In these cases there 
is little pus formed compared with the area involved. 

As a preventive of possible blood infection the following may be 
administered : 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 605 

1} — Hydrargyri bichloridi gr.j 

Tincturae forri ohloridi fjj — M. 

Sig. -Twenty drops in water four times a day. 

The editor employed this remedy with markedly beneficial effect, 
while suffering from a very severe abscess about the finger-nail, due 
to infection by the Streptococcus pyogenes and associated with 
lymphangitis extending as a bright red streak into the axilla. 

If the adynamia and other symptoms be progressive, medical 
cooperation should be obtained to divide the responsibility and to 
afford every means possible toward the cure. The extraction of the 
tooth followed by sterilization and curettement of the part, and the 
use of streptococcus antitoxin or vaccine conjoined with the 
sustention of the vital powers by nutritious predigested food and 
alcohol is logical. In even ordinarily severe cases not of this variety 
and there will be some fever due to the toxin absorbed, and the pain 
loss of sleep and appetite will cause physical debility. (See p. 149.) 

For this there is nothing better than the following, as tonic, anti- 
septic, and antipyretic: 

$— Saloli, 

Quininae sulphatis (vel hydrochloratis) . . . . aa gr. lx 
M. et fiant capsulas no. xx. 
Sig. — Take one four to six times daily, before meals when near them. 

Or, 

1$ — Quininse sulphatis gr. xxx 

Acetanilidi gr. xxiv 

Caffeinae citratis 5 gr. iij 

M. et fiant pil. no. xij. 

Sig. — One every hour. (Endelmann.) 

The facial swelling resolves with the cure of the abscess or its proper 
venting, but may be assisted by cold applications or cataplasma 
kaolini to the outside of the face and by gentle massage by the 
patient or nurse. 

As a means of reducing swelling, vibratory massage is useful. A 
simple appliance for this purpose, devised by W. H. Mitchell, 1 
consists of a cam-like piece of metal perforated at its smaller end for 
mounting upon a screw T mandril; it is held in the dental hand piece 
strapped to the hand as shown. Its centrifugal force imparts a 
vibratory motion to the hand which can be utilized for massage with 
the finger tips, or by holding in the hand an instrument containing 
upon its end a soft rubber cup. The part to be massaged should 
be lubricated with vaselin (Figs. 552 and 553). 

1 Dental Brief, 1908; Academy of Stomatology. 



606 



SEPTIC APICAL PERICEMENTITIS 



The heat of a large electric lamp concentrated upon the face from 
a short distance and followed by massage is also useful in facial 
swellings due to cellulitis. 



Fig. 552 



Fig. 553 





W. H. Mitchell's vibrator strapped to W. H. Mitchell's vibrator and rubber 



hand. 



cap applicator. 



Under no circumstances should hot poultices be applied to the 
outside of the face, as a discharge of pus in that direction will cause 
a disfiguring scar. If an abscess threaten to open externally, the 
abscess should be opened by an incision made from a point within 
the mouth, and, after sterilization of the tract, a drainage tent of 
antiseptic gauze should be introduced nearly to the bottom of the 
pus cavity. This should be removed daily, the abscess cavity steril- 
ized, and the tent renewed. An antiphlogistic compress should be 
applied to the face. The principal object sought is the mechanical 
apposition of the walls of the abscess cavity at the dependent or 
external portion, in order that these shall unite by granulation and 
that the fistula shall in this manner become an ordinary one. The 
patient should lie in a position to counteract the natural effect of 
gravitation. 

After lancing, the mouth should be kept well sterilized by frequent 
sprays or gargles of hydrogen dioxid, which may be diluted to one- 
third strength with water — i. e., to a 1 per cent, solution. 

If, in connection with the lower third molar, marked swelling be 
observed in the submaxillary triangle, free incision of the tissues of 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 607 

the floor of the mouth should be made at the angle of junction with 
tjie bone. The cut should be made close to the bone and toward it, 
but not too deep, lest the mylohyoid artery or nerve be injured. 

The deep lancing of an abscess upon the hard palate may cause 
a cut to be made in the posterior palatine artery. External to the 
jaws the facial and coronoid arteries are to be considered. Keeping 
close to the alveolar process while the cheek is pulled out renders 
the operation safe. 

It is ever to be borne in mind that so long as the cause of infection 
remains pus formation continues, and so long as pus forms tissue 
destruction is in progress; furthermore, in proportion to the amount 
of tissue loss perfect recovery after alveolar abscess is delayed or 
imperfect. 

While it is the clinical experience of nearly every operator that 
a tooth and adjacent structures may recover from inflammation 
which involves not only the first tooth attacked, but by an extension 
of the inflammatory process involves the general periosteum and 
neighboring teeth, provided the case receive prompt and decisive 
surgical treatment, yet the danger of necrosis and septicemia in 
prolonged cases is always imminent. When the general periosteum 
is involved, as shown by extensive boggy swelling in the mouth, if 
several free incisions carried to the bone do not afford prompt relief, 
the tooth which is the centre of infection should be promptly ex- 
tracted. If, in the continued course of the pericementitis, chills, 
followed by fever, a coated tongue, and much physical depression 
occur, a general infection is to be feared, and no time should be lost 
in sterilizing the mouth, extracting the tooth, and subjecting the 
socket to free spraying with antiseptics. Systemic treatment is to 
be given (see p. 605). 

In cachectic individuals acute abscesses may cause inflammation 
of the deeper tissues and of the periosteum as well, and extensive 
necrosis may occur. The after treatment of acute apical abscess 
which has been relieved by abortion is exactly that of moist gangrene 
or of chronic abscess without fistula (which see). In very mild 
cases the formaldehyd treatment may be instituted at once. In 
severe cases it is better to allow drainage for a day or two. When 
the relief has been afforded by lancing the treatment is as for chronic 
abscess with a fistula (see p. 618). 

Acute septic apical pericementitis may occur on a temporary tooth, 
most frequently a temporary molar. The symptoms and pathology 
are the same, except that the looser character of the alveolar struc- 
ture seems to frequently permit the abscess to assume the chronic 
form before the dentist is consulted. Children often hide these 



608 SEPTIC APICAL PERICEMENTITIS 

conditions from their elders out of fear of the dentist. In strumous 
children the inflammation may be spreading and the lymphatic 
glands may be involved. There may also be some symptoms of 
septic intoxication evidenced by chills accompanied by fever, etc. 
These cases require an opening of the abscess, sterilization of the 
part, and attention to the systemic condition. If seen in the acute 
stage the treatment is the same as for the permanent teeth, unless 
the disease occur shortly before the date for eruption of the per- 
manent successor, when the temporary tooth should be extracted, 
If treated, the canals should be filled with materials which can be 
resorbed by the tissues, such as paraffin or wax with aristol, para- 
form, or thymol (Fig. 587). 

As soon as the pus escapes, the condition of chronic apical abscess 
is established. 



CHAPTER XX. 

CHRONIC SEPTIC, PURULENT, APICAL PERICEMEN- 
TITIS (CHRONIC APICAL ABSCESS) 

By this title is meant a condition of apical pericementitis due to 
septic influences in which pus is continuously formed at the expense 
of the apical pericementum and contiguous tissues. It is the usual 
outcome of acute apical abscess, and is established as soon as the 
pus finds vent either through the gum as a natural or operative 
result, or through the root canal as the result of opening the canal. 

These two avenues of pus escape give the two clinical conditions of 
(1) chronic apical abscess discharging via the root canal; (2) chronic 
apical abscess with fistula: (3) a third condition of latent chronic 
apical abscess (true blind abscess) with absorption of pus by the 
tissue may exist. 



CHRONIC APICAL ABSCESS DISCHARGING VIA THE 
ROOT CANAL. 

Pathology and Morbid Anatomy. — First Grade. — Upon abortion of 
an acute abscess in the first stage the pressure of pus upon the apical 
tissues is released, and, as a rule, the walls of the abscess cavity 
throw out granulations which fill it. This tissue tends to organize 
into more or less healthy tissue (cicatricial tissue). The bacteria 
are killed out except at that part represented by immediate contact 
with the root foramen; at this point the tissues are infected and 
some molecular loss of tissue as pus may occur. A limited loss of 
granulation tissue by pus formation is compensated for by the 
formation of new granulations. The conditions are almost analogous 
to those existing in moist gangrene of the pulp, and require analogous 
treatment. 

Second Grade. — If the abortion of the abscess has only partly 
permitted the pus to drain, or the alveolar walls or crypts of the 
aBscess wall remain infected, the pus will continue to form and 
escape in some degree via the canal. If the tooth now be extracted, 
a small abscess sac will be found upon the root end. If opened, 
39 . (609) 




610 DISEASE OF PERICEMENTUM BEGINNING AT APEX 

this will be seen to be a mass of fibrovascular tissue (inflamed peri- 
cemental apical tissue) having a central lumen connecting with the 
root canal (the abscess cavity). 

Third Grade. — With partial vent to the pus formed, the abscess 
cavity of the second grade may enlarge, involve the bony walls of 
the alveolus, and the soft tissues then pro- 
Fig. 554 liferate to such an extent that they finally 

organize into a large, fibrous, vascular sac 
attached to the tooth. This sac has the 
central pus cavity before described, which is 
connected with the pulp canal. It may be 
a half-inch or more in length (Fig. 554), 
and may be extracted with the tooth or 
may be left attached to the bone. It neces- 
sarily occupies in the latter a cavity of a size 
ttodTradeTtf! abscess corresponding to its own bulk. As its inner 
sac containing a central walls are infected, extraction without its 

pus cavity; D, apex of i 1 • p , i i • i ±. 

root; c, canal containing removal leaves an infected area, which must 
pus. be disinfected or a secondary acute abscess 

may result. (See p. 603.) One case which 
had given only slight uneasiness owing to partial vent, was treated 
at two o'clock and the tooth extracted at midnight, had the appear- 
ance shown in Fig. 554. 

Fourth Grade. — Instead of organizing, the fibrovascular tissue 
may be liquefied into pus. The root apex becomes denuded for a 
distance about the apical foramen. Pus collects about the apex of 
the root and rests upon the bone, owing to the influence of gravity. 
The bone is thus infected, inflamed, and further liquefied, while 
necessarily the abscess cavity enlarges. If a bistoury be thrust 
through the labial alveolar wall in such a case, as shown in Fig. 555, 
but slight resistance will need to be overcome. In the low r er jaw the 
tendency is to burrow into the cancellated tissue of the bone away 
from the tooth, so that destruction of the pericementum may not 
be very extensive. In the upper jaw the tendency is to spread 
along the pericementum and into the cancellated bone, so that the 
cavities of chronic abscess upon the upper anterior teeth particularly 
may cause extensive excavation in the palatal process of the superior 
maxillary bone (Fig. 557). The pus may burrow in irregular and 
circuitous directions until it finds external vent. 

In long-established cases deposits of pus calculi (serumal) may 
form upon the root end (Fig. 558). The cement corpuscles of the 
apical cementum may die and the root tissue itself become infected. 
In other cases resorption of the root end occurs. (See Resorption.) 



CHRONIC APICAL ABSCESS 



(ill 



Symptoms. — In all of these cases the formations are gradual, owing 
to the partial vent, and it may be that no pain beyond a slight 



Fig. 555 



Fig. 556 




Chronic abscess on upper incisor, showing 
tendency of pus progressively to destroy peri- 
cementum, owing to the influence of gravity. 



Chronic abscess upon lower tooth, 
showing tendency of pus to sink 
into the substance of the lower 
maxilla, owing to the influence of 
gravity. 



gnawing or feeling of fulness or an occasional reflex pain may occur. 
If for any reason the vent become occluded, the pus formation 
becomes rapid and an acute abscess is set up, which may be painful 



Fig 557. 



Fig. 558 





Chronic apical abscess discharging 
through the hard palate and threatening 
to discharge labially. 



Chronic abscess, showing ' de- 
nudation of apex of root (a to 6), 
with deposits of calculi (a) upon 
cementum. 



or not, according to the amount of tension produced before discharge 
of the pus. Aside from this, the gum color at the apex is somewhat 



612 DISEASE OF PERICEMENTUM BEGINNING AT APEX 

deepened, the tooth is slightly loosened, and slightly tender to 
percussion. Signs of previous moist gangrene are in evidence. 

Diagnosis. — The passage, without production of sensation, of an 
undue length of fine probe into a canal is evidence of destruction of 
apical tissue and a guide to its probable extent. 

An extensively inflamed gum tissue over the apex indicates a 
probable approach of pus formation to gum tissue. The presence 
of pus in the canal or upon several dry cottons introduced for absorb- 
ent purposes is diagnostic. If pus be not seen, and the canal be 
thoroughly sterilized and dressed with an antiseptic, the supervention 
of an acute abscess affords evidence of the presence of an abscess 
sac or cavity. The x-rays afford a means of diagnosis (Fig. 571). 

Prognosis. — The prognosis is favorable to a cure in nearly all of 
these cases, provided thorough canal asepsis and filling can be 
attained and the abscess cavity can be drained and disinfected. In 
cases resisting this treatment, a fistula must be established. 

Treatment. — The first and second grades of chronic apical abscess 
discharging via the canal may be treated upon exactly the same 
principles which are involved in the treatment of moist gangrene 
of the pulp. The infection is considered as simply more deep seated, 
so that it is necessary to pass disinfectants into the abscess cavity 
with two objects in view: (1) To destroy the bacteria present; (2) 
to stimulate the tissues to granulative activity. The canal should be 
scraped and the foramen very slightly enlarged if necessary with a 
fine Donaldson cleanser, the canal having been flooded with 10 per 
cent, formalin or formocresol as an antiseptic. 

If necessary the root canal may be otherwise enlarged. (See p. 545.) 

A dressing of 10 per cent, formalin or phenol-camphor to which a 
little menthol and a drop of formaldehyd, 40 per cent., have been 
added, or formocresol, should be loosely placed in the canal and the 
tooth sealed for twenty-four hours, or, if the tooth has been very 
troublesome and is still tender, a soft temporary stopping may be used 
and the patient provided with instruments suited to the removal of 
the covering and the cotton. It is better that the tooth should be under 
the control of the patient. At the next sitting the cement stoppings 
are more tightly made. The Zieler-Hoffendahl method may be used 
to sterilize the root and abscess, then the dressing is sealed in for a 
few days and renewed as necessary, being made continuously tighter. 
(See p. 613.) When no pus can be found on the dressing or follow- 
ing it, or on an exploratory cotton twist, and there is no odor, the 
root may be filled; in case of any doubt in fine roots, with a removable 
material such as forma-percha on cotton or the paraform alum 
paste (p. 552), which may remain if no ill-results follow. A tern- 



CHRONIC APICAL ABSCESS 613 

porary crown filling of gutta-percha should be used for a week or 
two. Each change of dressing should be preceded by sterilization 
of the cavity and bulb of the pulp chamber with a strong formalin 
solution to prevent reinfection of the apical tissue during the change, 
and it is well to use counterirritation directly after the root filling. 

It is always well when using an occlusal opening to close it with 
amalgam or cement after the first tentative dressing, while compres- 
sible dressings are in place, as even one heavy bite upon the covering 
may force the medicament into the apical tissue and renew the 
irritation. Slightly countersinking the orifice of the tap will pre- 
vent an inward thrust of a rigid covering overlying cotton (Fig. 
532). 

Some operators prefer to leave a small vent in the temporary 
covering, used to act as a drain. This, however, is apt to prevent 
the concentration of the action of the medicament upon the apical 
tissue. If formaldehyd be irritant, perforating the temporary 
stopping with a pin will sometimes relieve the pressure. 

If pus formation persist in any case with a large foramen the cotton 
may either be protruding from the root and keep up irritation or 
fall short of the root end and permit pus to enter the canal, and 
especially if no pain has been produced, good results sometimes 
follow a departure to the immediate method of root filling. The 
canal and pus cavity are resterilized for a half -hour using formocresol, 
deliquesced zinc chlorid, or carbolic acid on cotton against the apical 
tissue, and the canal apex is then filled with gutta-percha or oxy- 
chlorid of zinc. The tissues are expected to care for themselves. 
A persistent discharge of serum or of glairy lymph is indicative of 
inflamed aseptic but weeping tissue, and requires the same treat- 
ment. (See p. 579.) 

In a relatively few cases teeth cannot be closed at all without a 
recurrence of trouble within a short period, which trouble is usually 
relieved by opening the tooth. The repetition of this is annoying; 
and in some cases is due to the strength of medicaments such as 
formaldehyd, w T hich should be modified or abandoned for sedative 
antiseptics such as phenol-camphor or eugenol plus menthol. In 
some of the cases the gases may accumulate more rapidly than 
disinfection occurs. In other cases the irritability of the tissues 
seems to produce intolerance of any remedial measures. What is 
known as "systematic stopping and unstopping" seems sometimes to 
overcome the irritability and accustom the tissues to being covered. 
The system consists of stopping with eugenol and menthol or modified 
formocresol for about eight hours, or from morning to afternoon, 
then venting and redressing until the following morning, then for 



614 DISEASE OF PERICEMENTUM BEGINNING AT APEX 

twenty-four hours, then forty-eight, then seventy-two, etc., until 
the tooth stays stopped. 

There have been a few patients who cannot seem to have teeth 
" treated," nearly all cases being practical failures even when aseptic. 
Some few may be kept in comfort for a while with permanent vents, 
but this is objectionable. The making of an artificial fistula should 
be attempted. 

Cyst formation occurs owing to the projection of an aseptic root 
filling or to some not well understood cause; a cystic swelling may 
occur over the root of a tooth and have its origin in the pericementum 
The swelling is apt to be bluish about its margin, and has a clear, 
stretched look in the centre. It is probably due to a collection of 
fluid in some portion of the pericementum, or may have as its excitant 
a portion of calculus deposited aseptically in the pericementum. 
Indeed, apart from infection, it may be that cases of pericemental 
abscess, discharging merely glairy fluid, are cystic swellings. It may, 
however, be in relation with septic canal contents. (See p. 631.) 

In such a case, if swelling increase or be persistent, an artificial 
fistula must be established (see p. 601) and the case treated as a 
chronic apical abscess with fistula. 

In the third and fourth grades the prognosis for treatment by way 
of the canal is not, as a rule, good, but if desired may be attempted. 
If, however, an artificial fistula be established, the ease of treatment 
is greatly increased. The case is then treated as a chronic apical 
abscess with fistula. 

In no case should hydrogen dioxid be forced in quantity into the 
pus occupying such an abscess cavity until the fistula has been made, 
and it is better even then that the bulk of it be washed out with warm 
water before applying the drug. A neglect of this precaution may 
bring about great pain, owing to the rapid reaction of the hydrogen 
dioxid with the pus and blood present. In some cases hydrogen 
dioxid has forced pus into remote locations without destroying it. 

CHRONIC APICAL ABSCESS WITH FISTULA. 

Morbid Anatomy and Pathology. — This form of chronic abscess 
occurs as the result of the discharge of an acute abscess through the 
gum or other part of the surface of the body, and whether the fistula 
has naturally occurred or been artificially established. (The interior 
of the mouth or other cavity exposed to contact with the air is 
considered external to the body proper.) 

If the acute abscess has been severe or long continued, the tissue 
destruction may be great, but, as a rule, granulation promptly sets 



CHRONIC APICAL ABSCESS WITH FISTULA 



015 



in and the walls of the abscess cavity organize into cicatricial tissue. 
From the interior of this a canal (fistula or sinus) lined with cica- 
tricial tissue leads to the surface, the pus being almost constantly 
formed at the expense of the granulation tissue, which is as constantly 
renewed. 

The fistulous opening, as a rule, appears as a small teat of inflamed 
tissue located, in the majority of cases, upon the buccal surface of 
the gum, about a quarter of an inch below the apex of the root and 
slightly distal to it — a position probably determined by the density 
of the tissues surrounding the acute abscess. At times the only 
evidence of a fistula is a small spot of inflammation surrounding a 
minute opening, from which pus exudes. The fistula is sometimes 
located upon the lingual surface of the gum. It may perforate the 



Fig. 559 



Fig. 560 





Chronic apical abscess on mesial root. 
Ultimate result of a pulp capping. Editor's 
practice. (Skiagraph by Hagopian.) 



bone of the hard palate and open 
through the mucous membrane of 
the roof of the mouth (Fig. 557). 
Instead of finding exit by a direct 
path through the buccal or lingual 
alveolar plate and gum, the pus 
may burrow along the length of 
the pericementum and discharge 
at the neck of the tooth, and sim- 
ulate a pyorrhea pocket (Figs. 542 
and 543) . One-half or more of the 
lateral aspect of the pericementum 
may remain vital, although involved 
in* a chronic inflammation, the remainder being destroyed. Not in- 
frequently the pus burrows along the surface of the bone and dis- 
charges at a point over an edentulous portion of the jaw. This is 



Chronic alveolar abscess of the root 
of a lower incisor, with abscess cavity 
passing through the body of the bone 
and discharging on the skin beneath 
the chin: a, very large abscess cavity; 
b, mouth of the fistula. (Black.) 



616 DISEASE OF PERICEMENTUM BEGINNING AT APEX 

common to a lower bicuspid. It may burrow in the direction of 
the apices of other teeth, destroy their pulps and thus cause an 
abscess, having added causes for persistence. 

When the apices of the roots of upper posterior teeth lie in very 
close proximity to the floor of the antrum, perforation of this floor 
may occur before tissue destruction has proceeded far enough in 
other directions to afford escape to the pus (Fig. 545). Extensive 
pus accumulations may occur in the antrum in consequence, and 
when the tissues in the antral floor are affected, other teeth may be 
involved. It may discharge into the cavity, in connection with 
acute abscesses; at such points the discharge may remain persistent. 
Sometimesjthe^discharge occurs through the canal of the affected 
tooth; the canal then acts as a fistula (Fig. 538). Upon a lower 



Fig. 561 



Fig. 562 





Fistula passing down through the body of 
the lower maxilla. (Black.) 



tooth, particularly the incisors, the 
pus may burrow downward through 
the cancellated tissue of the bone 
and emerge at the base of the bone 
and open upon the face (Figs. 560 and 
561). 

In other cases the pus may per- 
forate the bone and find passage 
along the submuscular tissue, open- 
ing upon the face or neck (Fig. 
562). The apices of the roots of 
teeth lying beneath the line of in- 
sertion of the mylohyoid muscle may cause an abscess to open in 
the neck cavity. Cryer records a case where an abscess opening 
upon the face immediately anterior to the line of the facial artery 



Chronic alveolar abscess at the 
root of a lower incisor, with a 
fistula discharging on the face under 
the chin: a, abscess cavity in the 
bone; b, b, b, fistula following in 
the periosteum down to the lower 
margin of the body of the bone and 
discharging on the skin. (Black.) 



CHRONIC APICAL ABSCESS WITH FISTULA 617 

was traced to the root of a lower molar; the direction of the sinus 
is shown in Fig. 563. In a case having a similar anatomical associa- 
tion the pus penetrated the bone lingually, was encapsuled beneath 
the internal pterygoid muscle, and appeared as a swelling at the 
inner aspect of the angle of the jaw. Another case dissected along 
the muscles of the neck and discharged at the clavicle. Occasionally 
the apices of the roots of lower molars are separated from the inferior 
dental canal by only a thin lamina of bone, so that discharge into 
this canal may occur with infiltration along the vessels and nerves 
in the canal (Fig. 254). While discharge into the nasal chamber 
is most frequently associated with abscess upon the central incisors, 
abscesses upon molars may discharge into the same cavity. 

Cementum infection occurs as a sequence to death of the cement 
corpuscles from lack of nutrition. Pus calculi may also form on the 
roots in the long continued cases. The granulation tissue springing 
up about the parts has a resorbent action and the root ends are 
often resorbed, though this action is probably to an extent counter- 
acted by the alkalinity of the pus. The formation of the latter may 
however, be in abeyance at times. 

The extent of tissue destruction varies considerably, but is usually 
greatest in dependent parts, gravity influencing the burrowing of 
the pus. 

Symptoms and Diagnosis. — A fistula is seen upon the gum, visible 
as either a small teat of flesh (perhaps pedunculated), discharging 
pus, or as a tiny orifice in the gum surrounded by inflamed tissue, 
and from which pus may be squeezed (Fig. 544). As a rule, a soft 
silver probe may be passed to the apex of a nearby root, whether 
possessing a crown or embedded in the bone. In case of an external 
opening upon the face a similar procedure shows the trouble to lie 
with some tooth root. The x-rays will sometimes be valuable in 
determining the exact location of the abscess cavity. 

Upon the teeth themselves but four conditions may cause a fistu- 
lous opening: (1) Moist gangrene of the pulp or its equivalent apical 
infection; sometimes the sinus is at the oral end of a broken root; 
(2) septic perforations, apical or lateral; (3) a pericemental abscess 
(see Pericemental Abscess); or a secondary abscess associated with 
a pyorrhea pocket (see Pyorrhea Alveolaris); (4) lateral abscess 
about a third molar or impacted tooth. 

Aside from these, the probe may lead to carious or necrosed bone, 
a, cyst, or a subperiosteal abscess (maxillary periostitis). 

In these cases the probe does not lead to a root. Carious bone 
will impart a honey-combed sensation to an excavator; necrosed 
bone will be exposed and firm, or the sequestrum will be in evidence 



618 DISEASE OF PERICEMENTUM BEGINNING AT APEX 

as a movable body. There may also be several fistulas and extensive 
inflammation of the tissue. A cyst will be a tumor with certain 
characteristics, and an impacted tooth will usually impart the feel 
of smooth enamel to the instrument, though the enamel may at 
times be rough at certain points. An embedded root will be movable, 



Fig. 563 



Fig. 564 




Abscess with tortuous sinus, open- 
ing upon the face: A, tissue of cheek; 
B, floor of mouth; C, abscess tract. 

Fig. 565 





Large abscess cavity in relation with a 
lateral incisor, complicated by an im- 
pacted supernumerary tooth beneath the 
nasal spine. (Philadelphia Dental College 
Museum.) 



and will present the dentin and its 
central opening, the pulp canal, 
as diagnostic features. Maxillary 
periostitis will, as a rule, have a 
history of traumatism, or the pre- 
vious use of a probably infected 
hypodermic needle 1 associated with 
it. In all cases not clearly due to other than dental causes, evi- 
dence of the four dental conditions mentioned should be sought. 

Treatment. — In cases arising from sources not dental, surgical 
interference for the removal of the cause is necessary. This may 
require a minor or major operation, according to the case. 

In the purely dental cases the cause must also be removed. If 
due to pericemental abscess, this is to be treated. If due to a septic 



Abscess and resorption at apex. 
(Skiagraph by Lodge) 



Boenning, Dental Cosmos, 1902 



CHRONIC APICAL ABSCESS WITH FISTULA 619 

perforation not yielding to treatment by way of the root canal, 
the fistula may be enlarged, packed open with antiseptic cotton or 
gauze applied on successive days, and when the perforation is exposed 
it may be filled with amalgam. If property done the fistula should 
heal. If this operation be impossible, the root should be amputated 
at a point between the perforation and the crown. If the perforation 
be in the middle or cervical third of the root, it may at times be 
treated from the root canal. A good method is to force root-filling 
material through the perforation and fistula and to smooth it off 
through the sinus. Stiff oxychlorid of zinc or oxyphosphate of 
copper are excellent. If incurable, the entire root must be amputated 
in case of a multirooted tooth. In case of a single-rooted tooth 
the tooth must be extracted, and if the conditions warrant the 
operation the root may be perfectly sterilized, properly filled, and 
then replanted after the associated abscess cavity has been surgically 
obliterated. (See p. 624.) 

In the cases due to moist gangrene of the pulp the canals must be 
freely entered, the apical foramen opened with Donaldson or other 
cleansers, and the canals and abscess tract thoroughly sterilized. 

The canals are flooded with a formaldehyd solution, mechanically 
enlarged, and if possible made continuous with the abscess cavity. 
It is then filled with hydrogen dioxid. With a Swiss broach upon 
which cotton is wound a plunging force is exerted upon the fluid in 
the canal. This tends to drive it into the abscess cavity and out of 
the fistula, flushing and sterilizing the abscess tract. This is then 
repeated. Antiseptic liquid soap may be used. If this simple pro- 
cedure be not effective, a thread of cotton saturated with carbolic 
acid should be placed in the canal. Pressure is then exerted with 
gutta-percha, as in pressure anesthesia. A bit of cotton roll should 
be used to guard against burning the tissues. Phenolsulphonic acid 
may be forced through the apical foramen and fistula in some cases. 1 
This dressing may be left until the next visit. A third method con- 
sists of filling the crown cavity with gutta-percha or vulcanite 
rubber, forcing the nozzle of an abscess syringe through the mass, 
and driving down the piston of the syringe. In all these procedures 
except the initial sterilization, the unaffected roots of multirooted 
teeth are to be avoided so far as possible, as undue pressure may 
excite an abscess The fistula will admit the nozzle of the syringe, 

1 Acid phenolsulphonic consists of 97 parts, by weight, of concentrated sulphuric 
acid and 93 parts, by weight, of phenol, kept at 100° C. for about twenty-four hours 
to produce a reaction, when sufficient distilled water is added to make the liquid 
assay about 80 per cent, of phenolsulphonic acid. (Buckley, Lilly.) Prinz, in Cosmos, 
April, 1912, gives some good reasons for its inferiority for any purpose to sulphuric 
acid. 



620 DISEASE OF PERICEMENTUM BEGINNING AT APEX 



Fig. 566 



Fig. 567 




Minim syringe. J. N. Farrar's alveolar abscess syringe. 

Fig. 568 




Bulb syringe. 



CHRONIC APICAL ABSCESS WITH FISTULA 621 

which may be used to flush out the abscess tract with hydrogen 
dioxid. 

The nozzle of a hypodermic needle may be fitted to the canal by 
packing wax, temporary stopping, or raw vulcanite about it; a piece 
of flexible tubing may be previously stretched over the free end and 
later the other end of the tubing stripped over the compressed-air 
syringe. Medicaments or air may thus be blown through the fistula. 
The method should be cautiously used in fistulous cases only, except 
for reasons well known by the operators employing them, as very 
painful distention of the cheek may occur. (See p. 576.) 

The rubber cup shown in Fig. 569 may be used as a vacuum pump 
to draw the pus from the fistula or to draw medicaments through 
the canals. 

All preliminary work having been done as well as possible, formo- 
cresol is to be pumped into the abscess tract and the canal tempor- 
arily stopped with the same antiseptic on cotton. With this treat- 
ment the discharge of pus should cease and be replaced by serum. 
It is good practice to resterilize the canal and fill it as soon as this 
result is noted, or, in emergency cases, the canal may be filled at 
the first sitting after prolonged germicidal work. The fistula then 
will probably heal uninterruptedly in the vast majority of cases. 
In a week or two the fistula should have healed if attached to treat- 
able canals; for the difficult canals subjected to germicides only more 
time may be required, but healing usually eventually occurs owing 
to the removal of the cause. 

If the abscess cavity does not heal one of several causes may 
be assigned: (1) The crypts in the walls of the abscess cavity may 
require further disinfection; (2) the cotton in the canal may have 
absorbed pus formed after an interval of antiseptic influence and 
may keep up the infection; (3) the root canal may not be explorable; 
(4) the root end may be encrusted with calculus, or the cementum be 
infected, or dead bone may be present. 

For the first condition the canal and- abscess tract may be treated 
with 10 per cent, zinc chlorid, or mercuric chlorid may be added 
to hydrogen dioxid (1 to 500 or 1 to 1000) and the abscess cavity 
syringed out at intervals. For the second condition a non-absorbent 
dressing should be used, such as forma-percha, or the root apex 
may be permanently filled with gutta-percha. In the fine, unex- 
plorable canals 25 per cent, pyrozone may be used for twenty-four 
hours, as though bleaching the root, or Rhein's cataphoric method 
(see p. 556) may be employed. In some cases abscesses require 
some weeks to heal, but eventually do so, particularly if the abscess 
be syringed out with an antiseptic every third day via the fistula, 



622 DISEASE OF PERICEMENTUM BEGINNING AT APEX 

and the abscess tract filled with balsam of Peru or paraffin and 
aristol. Beck's bismuth paste may be injected for skiagraphy or to 
stimulate the fistula. Opening the fistula daily with a probe or 
needle aids healing from the bottom out. 

Tissues about abscesses have an inherent tendency to repair; cases 
of long standing frequently healing promptly, sometimes, though not 
often, in twenty-four hours. 1 

In indolent chronic inflammation the use of a small gum dry cup 
with vacuum bulb attached may be used for five or ten minutes 
at a time several times a day, to draw fresh blood and effusions 
into the inflamed part. The opsonic index of the lymph drawn 
in is said to be raised to several times beyond that of the body lymph, 
thus rapidly increasing phagocytosis in the part. The rubber cup 
shown in Fig.- 569 may be left imperforate and furnished the patient 
for this purpose. 



Fig. 569 



Fig. 570 





Rubber cup to be used as a 
vacuum cup. 



Amputation of root apex: OG, opening in 
the gum made by packing fistula; AC, 
abscess cavity; RF, root filling. 



For the fourth class of cases the apical foramen should be sealed 
and the abscess tract syringed once a week with 25 per cent, sul- 
phuric acid, the mouth and clothing being properly protected by 
using a pad of cottonoid over the fistula and needle to absorb the 
excess. This dissolves calculi and disinfects dead cementum. It 
also stimulates the soft parts to a granulative action. If necessary 
the patient should receive appropriate systemic treatment, especially 
if anemic. (See p. 637.) In this way some old and somewhat obsti- 
nate cases may be induced to heal. In some cases gravity so retains 
pus in abscess cavities that granulation is interfered with. The 



Darby, Proceedings of Academy of Stomatology, Philadelphia, 1899. 



CHRONIC APICAL ABSCESS WITH FISTULA 



C323 



instruction of the patient in the syringing out of the tract with a mild 
antiseptic several times a day is of great value in that it removes 
pus which if retained would destroy granulations. Hydrogen dioxid 
should not be used except in small abscesses as it may cause the 
forcing of pus to distant areas. Many apparently desperate cases 
heal of their own accord after some months. Some success attends 
the packing of a root with a thick paste of iodoform in any oil after 
opening the root as far as possible. Cases in which a canal was not 
explorable for any considerable distance have healed after this treat- 
ment. The .T-ray application, made for ten or twenty seconds, or ski- 
agraphy seems to aid the healing of the fistula. The high frequency 
current also is a stimulant. If the abscess be incurable by the 
above method, or radical measures being considered better, the root 



Fig. 571 



Fig. 572 



Fig. 573 





A skiagraph of apical 
abscess cavity about two 
root apices; incurable 
by ordinary means. 




The same after root 
amputation. 



The same thirty 
days later, showing 
a certain amount of 
new bone formation. 
(Price.) 



end may be amputated, after canal filling as far as possible with 
gutta-percha. The fistula is enlarged and packed open with anti- 
septic gauze or cotton, or sandarac varnish dipped into powdered 
orthoform applied until the root end is fairly in view. After steril- 
ization of the abscess cavity and local anesthesia, a dentate fissure 
bur or a Schamburg surgical bur is laid upon one side of the root at 
the level of the healthy tissue, and carried laterally with a sawing 
motion until the root end is separated. It may readily be picked 
out. If the root can be correctly located without packing the fistula 
the part may be anesthetized and a portion of gum may be cut away 
with a tubular knife, or an incision may be made, after which a 
fissure or surgical bur may be used to cut away the root. Any 
necrosed bone may be removed at the same time. A skiagraph 
to act as a guide is necessary when the fistula is not packed open. 



624 DISEASE OF PERICEMENTUM BEGINNING AT APEX 

Necrosed root ends may occasionally be seen projecting through 
the gum and alveolar process which have been lost above them. 
They should be removed as above indicated. Sometimes salivary 
calculus deposits on them. 

Antiseptic gauze or cotton saturated with balsam of Peru should 
be packed into the abscess cavity after operation to stimulate granu- 
lation. The quantity of gauze should be gradually lessened until 
the cavity is nearly healed. It should thereafter be kept sterilized 
by means of hydrogen dioxid until the cavity has healed. An 
alternative is to inject into the cavity Beck's bismuth paste: 

1$ — Bismuth subnitrate 30 parts 

Vaselin 65 parts 

Paraffin 5 parts 

Wax 5 parts 

Mix while boiling. 

which excludes septic moisture, is antiseptic, and stimulates granu- 
lation. Stimulation by means of fused silver nitrate or sulphuric 
acid or scarification is at times necessary. Bone should gradually 
be deposited about the roots (Figs. 571, 572, and 573). Failure 
indicates some condition of sepsis; presumably the amputation has 
not included all septic root or the canal filling is defective. 

A still more radical method of surgical treatment involves the 
extraction and replantation of the root, if worth while. The mouth 
is sterilized and the tooth extracted, care beng taken not to injure 
the enamel with the forceps. It is then placed in a 1 to 1000 solu- 
tion of mercuric chlorid at 120° F., or phenol sodique, 20 per cent. 
The apex of the alveolus is in the meantime sterilized with hydrogen 
dioxid plus mercuric chlorid and thoroughly curetted. Bleeding is 
checked with the same solution or phenol sodique, 20 per cent., 
and a tampon of cotton saturated with the latter is packed into 
the alveolus. The replantation may be deferred for a few days if 
the parts are badly infected. In such case granulation is permitted. 

Returning to the tooth, the apex is cut off slightly beyond the 
denuded area and smoothed; the pulp canal is well opened from the 
apex, all debris removed from it, and it is then well sterilized with 
sodium dioxid or 25 per cent, pyrozone. The canal is then dried 
and filled entirely with gutta-percha, or partly with gutta-percha 
and the operation completed with gold, which is nicely smoothed. 
The tooth should be handled in an aseptic napkin or one wet with 
the antiseptic, and when ready should be returned to the sterilizing 
solution. All being ready, the tampon or granulations are removed, 
the tooth washed in sterile water and replaced in its socket, and a 
previously prepared retaining appliance cemented to place. This 



CHRONIC APICAL ABSCESS WITH FISTULA 025 

should remain for six weeks and be replaced should indications 
demand it. If the tooth be valueless for replantation purposes, 
the operation of transplantation may be done either immediately 
after extraction of the offending tooth or a few days later. The 
possibility of resorption of the root after plantations should have 
careful consideration, though it is not prohibitory. 

The operation of transplantation may be done with a tooth recently 
extracted from another mouth or with a dried tooth, or, preferably, 
one kept in alcohol and glycerin, which many extracting specialists 
habitually retain to oblige applicants. If a suitable tooth be not 
obtainable, a root may have a crown mounted upon it in such manner 
as to have an open joint at a point to be placed beneath the gum 
line, and this joint should be filled with cohesive gold and polished. 
The tooth root is, of course, sterilized previous to and after the 
crown mounting, and its canal should have been thoroughly filled 
with gutta-percha. Any of these may become firm if thoroughly 
splinted for a proper length of time. The alveolus should be made 
to fit the root snugly by means of a bone reamer. The operation 
of implantation differs from this only in the fact that it is done where 
a tooth alveolus has been obliterated by combined absorption and 
bone formation, as after extraction (see p. 142). If the tooth be 
not lost by resorption, it is probable that some resorption occurs — 
toleration then ensues and bony deposition in the bays of resorp- 
tion and about the root occurs. Possibly a true ankylosis (which 
see) may occur. 

To select a proper tooth make a model and bite from an impression 
taken before extraction or immediately thereafter, cut off the offend- 
ing tooth from the model, ream out a socket in the plaster; select 
tooth, and fit in place; attach with a little soft plaster, the model 
being thoroughly wet. Construct the retaining appliance, remove 
the tooth, sterilize, and fill the root; then put the tooth in the 
sterilizing agent until needed. Mendel- Joseph and Dassonville 1 
have shown that in case of removal of a portion of the pericementum 
the lost portion may be regenerated. 

Greenfield 2 has introduced an artificial root made cribriform of 
platinum soldered with pure gold. Special instruments of varied 
sizes are necessary to correspond with the sizes of the roots. Under 
due aseptic precaution the gum is cut with a tubular knife, and the 
socket drilled with a circular trephine, which preserves a core of 
bone, and the root covered with Beck's bismuth paste is inserted. 
Later a crown is mounted or a bridge attachment constructed. 

1 Dental Cosmos, 1906, p. 1059. 2 Ibid., April, 1913. 

40 



626 DISEASE OF PERICEMENTUM BEGINNING AT APEX 

The reader is referred to the article for details. The editor has had 
no experience with this method. 



Fig. 574 



Fig. 575 




*st&fa 



W+9 



III 




Tubular knife for 
cutting gum. 

Fig. 576 



Trephine with central 
starter later removed. 



Fig. 577 



Fig. 578 



Trephine with cen- 
tral starter removed. 

Fig. 579 







Artificial socket Artificial root and 
drilled in bone, a crown separated, 
core being left. 



Artificial root 
with crown in 
place. • 



Artificial 
place. 



root in 



Several cases of fistulous openings into the antrum have been 
noted by canal exploration in which no history of discomfort from 
antral empyema could be obtained. It was assumed that the root 
ends approximated the floor of the antrum, and that the abscesses 
were of simple chronic type. Such cases were treated upon the 
common principle of canal antisepsis, flushing the abscess tract 
with an antiseptic, and filling the canals. The antral condition 
was explained to the patients, who were warned of possibilities, but 
such as yet have not been reported. 



CHRONIC APICAL ABSCESS WITH FISTULA 



627 



A chronic abscess may discharge into the maxillary sinus for a 
long period before being discovered, unless the pus accumulation be 
extensive, when it escapes from the antrum into the cavity of the 
nose, discharging by one side. Smaller accumulations of pus find 
exit in the recumbent position, and attention is called to one antrum 
as the seat of affection by noting that in the morning pus appears 
at but one nostril. The discharges from purulent nasal catarrh 
appear upon both sides. 

Fig. 580 




Two artificial roots in drilled sockets. Greenfield. (See text.) 



A more common history of antral empyema is the patient's com- 
plaint of dull, heavy pains and uneasiness over one side of the face, 
and an offensive odor, which may not be evident to the operator. 
High transillumination of the tissues about the mouth and through 
the cheek, by means of the electric mouth lamp of 20 volts capacity, 
the patient being in a dark room, may reveal an opacity on one or 
perhaps both sides, indicating the presence of fluid in the antrum. 
A clear pinkish transillumination is a sign of health. Tumors in the 
antrum entirely obstruct the light. Examination of the posterior 
teeth will show one of them to be pulpless, if the cause lies in apical 
abscess. If such a tooth be extracted, a profuse flow of pus may 
follow, and a probe may be passed through an alveolus directly into 
the antrum. 

The diagnosis may be assisted by z-rays, both antra being radio- 



628 DISEASE OF PERICEMENTUM BEGINNING AT APEX 

graphed for comparison. Raper 1 states that the shadow does not 
actually demonstrate the presence of pus, but that something abnor- 
mal exists whether pus or a soft tumorous growth, the appearance 
being the same. It, however, locates the disease, whether in the 

Fig. 581 




A, antrum with pus in it. B, healthy antrum. (Radiograph by Carmen of St. Louis.) 
Courtesy of Dr. Howard R. Roper. 



antrum or other sinuses. The presence of opaque foreign bodies, 
as a piece of tooth root causing disease, is shown by skiagraphy. 
Although extraction is the usual surgical relief, dental conserv- 
atism rebels against the immediate condemnation of the offending 

1 Items of Interest, July, 1912. 



CHRONIC APICAL ABSCESS WITH FISTULA 



629 



Fig. 582 



tooth. Efforts at curing the antral condition through the pulp 
canal are well-nigh hopeless— the antrum is entered at some other 
point. The tooth is treated as any infecting root; is sterilized and 
tilled. The most certain spot of 
entry to the antrum is about one- 
quarter inch above the buccal roots 
of the upper first molar or between 
the roots of the first and second 
molar. The part, or the patient, 
is anesthetized, and the soft tis- 
sues incised or a section removed 
by means of a tubular knife; a 
drill or trephine at least one-eighth 
inch in diameter, driven rapidly, is 
passed upward, backward, and in- 
ward, piercing the thin shell of the 
antrum at this point. The opening 
is made of convenient size to admit 

of thorough exploration. The nozzle of an atomizer or syringe, filled 
with a mild antiseptic solution, is passed into the antrum and the 
cavity is freely sprayed. A probe or the finger is passed into the cavity 
and an exploration made to detect the presence of any dead bone or 




Emypema of antrum due to 
abscess upon root of bicuspid tooth. 
(Radiograph by Price.) 



Fig. 583 



Fig. 584 




Scar caused by alveolar abscess dis- 
charging on the face. (Black.) 




Operation for the remedy of scar on the face 
caused by alveolar abscess. (Black.) 



bony septi, which, if found, must be removed, the cavity of entrance 
being enlarged to permit their removal. The antrum is then packed 
with gauze impregnated with iodoform, etc. After a few days the 



630 DISEASE OF PERICEMENTUM BEGINNING AT APEX 

cavity is sprayed about every other day with very dilute, warm 
Dobell's solution, Lugol's solution, or sterile ocean water. (For further 
information see works on Oral Surgery.) The opening either heals 
of itself or may be made to do so by the use of caustics or stitching 
the parts. 

Unless necrosis of bone occur, cases of fistula opening upon the 
face or neck may be healed by the ordinary methods of canal treat- 
ment, carried out with extraordinary care to accomplish the irriga- 
tion of the fistula, or at least sterilize the apical tissue. The scar 
formation is less than when extraction is practised for the removal 
of the cause. If the fistula be indolent, the granulations may be 
stimulated by means of an injection of 10 per cent, silver nitrate 
solution. If the fistula obstinately refuse to heal, the tooth should 
be extracted and necrosed bone, if any be present, surgically removed, 
though amputation of the root apex may be tried. 

Flagg 1 suggested, as a means of lessening scar formation, that a 
seton be passed through the external fistula into the mouth, and that 
it be gradually drawn into the mouth as the external fistula heals, 
after which the tooth is to be extracted if otherwise incurable. 

In fistulae discharging upon the face the formation of scar tissue 
may bind the tissue of the cheek tight to the bone. When this 
occurs beneath the tip of the chin, the scar, after healing, usually 
resembles a dimple, and calls for no interference. The scar and 
binding down along the border of the inferior maxilla, or beneath 
the malar bone in the upper maxilla, may produce deformity calling 
for remedy (Figs. 583 and 584). Black's operation is to be performed 
to lessen the deformity, for its complete correction is not practicable. 
A finger placed in the mouth draws the cheek away from the alveolar 
wall, when the exact position of the cord of attachment is discovered. 
A tenotome knife is passed into the tissues, dividing the band of 
attachment; a long pin is passed through the most depressed portion 
of the scar, its centre, the long ends of the pin resting upon the 
face; strips of adhesive plaster laid upon the skin under the head 
and point of the pin will prevent the latter sinking into the soft 
tissues. The pin is retained for several days, until the cut in the 
mouth heals. The principle involved is the supplying of a new 
section of scar tissue which, while it shrinks, makes the total length 
of the cord greater, hence less binding. 

Systemic Complications. — The cachectic, debilitated, anemic, tuber- 
culous, and syphilitic are liable to extensive pus formation, which 
enlarges the cavity unduly and may involve the roots of other 

1 Lectures on Dental Therapeutics. 



CHRONIC BLIND APICAL ABSCESS 631 

teeth or even cause devitalization of their pulps, which aids in the 
continuance of the abscess by adding a fresh cause. 

In such cases all the dead pulps should be removed after careful 
diagnosis, and the patient should be instructed in the use of a Sub. 
Q. syringe and a mild antiseptic, the object being to keep the depend- 
ent parts free of pus and allow granulations to form rather than 
be constantly broken down. In such cases hydrogen dioxid should 
be avoided as it may force undestroyed bacteria into remote parts. 

In addition, such systemic medication or remedial measures as 
will raise the recuperative and resistant powers of the tissues should 
be employed. 

If very persistent, a vaccine may be employed, after the method 
of Wright, to raise the opsonic index. (See p. 63.) The direct results 
of infection, toxemic and septicemic, have already been considered. 
Grieves contends that many root ends remain necrotic and develop 
blind abscesses and their sequelae (which see). 

Chronic Blind Apical Abscess. — A true blind abscess is one with- 
out a point of discharge. It is a result of septic contamination 
from root canals, a condition in which bacteria in unfilled root 
apices or in the interspaces between a root filling and the canal 
wall find their way into the fluid entering such a space and produce 
putrefaction — a condition practically analogous to moist gangrene 
of the pulp; or else bacteria in the blood arising from some other 
source, dental, tonsillar, or other focus, or entering to form a general 
blood infection, enter an apical region previously weakened as by 
pulp removal, apical irritation by root canal filling, a previous abscess, 
etc., and -develops a chronic apical abscess. 

An apical abscess is formed and the apical tissue acts as a fibro- 
vascular envelope or sac. Under the pus pressure and the pumping 
force of masticatory movement, absorption of toxins and pus germs 
by way of the lymphatics occurs. The lymphatic glands may be 
involved; a systemic infection occurs. 

Hartzell 1 states that Rosenow has shown that streptococci 
found in the mouth and tonsils can be made under suitable condi- 
tions to change into typical and encapsulated lanceolate pneumococci; 
or under other cultural conditions to produce organisms which 
locate in the joints, causing arthritis deformans; and under still 
different cultural conditions to produce Streptococcus viridans which 
is the common organism in heart-valve lesions, and under still other 
cultural conditions to become capable of causing ulcers of the 
stomach and bowels. 

1 Journal of the Allied Societies, June, 1914 



632 DISEASE OF PERICEMENTUM BEGINNING AT APEX 

In animals Rosenow has experimentally brought about heart 
lesions, from the bacteria in these heart lesions has caused ulcer of 
the stomach. From the bacteria there he has caused joint affections. 
From these he has produced typical pneumonia, and from the lung 
removed the original strain of organism which was also tested out 
along the series. 

Hartzell has observed that when abscesses or pyorrhea pockets 
are freely communicating with air streptococci are most often non- 
hemolytic. In deep but active abscesses they are hemolytic. In 
long standing and blind abscesses they are non-hemolytic owing 
to encapsulation and the depressive activity of their own metabolic 
products. 

Hartzell, in support of transmutation of bacteria, cites Larsen 
as causing the fusibacillus to develop a typical spirillum and again 
relapse into the fusiform bacillus. (This may account for Vincent's 
fusibacilli and spirilli found in conjunction in Vincent's angina.) 

He quotes Schottmuller as isolating streptococcus mucosus from 
the lesions of parametritis, meningitis, and phlebitis and shows its 
biological characteristics as allied to those of pneumococcus. By 
experiments carefully conducted to exclude oral bacteria from septic 
root ends clipped into media, Hartzell developed streptococci which, 
entering the blood with their toxins, travel to distant points and 
produce systemic toxemia and local manifestations. It seems, 
therefore, reasonably clear that ordinarily harmless bacteria, as 
S. viridans and the fusibacillus, may transmute into virulent ones 
by a change in cultural conditions. 

According to Grieves 1 the following distant manifestations may 
occur, as the result of combined ingestion and absorption of pyogenic 
cocci and the production of a septicemia and toxemia: 

1. Upon the muscles, causing myositis. 

2. Upon the joints, causing arthritis, synovitis, etc. 

3. Upon the blood, causing septic and pernicious anemia and 
endocarditis or pleurisy. 

4. Upon the glands, causing lymphadenitis. 

5. Upon the nervous system, causing toxic neuritis and degenera- 
tion. 

6. Upon the organs of excretion, causing skin rashes and nephritis. 

7. Upon the gastro-intestinal tract, causing septic gastritis, enter- 
itis, cholecystitis, appendicitis, colitis, etc. 

In the kidney lesions, Hartzell notes albuminuria and casts in 
quantity, lessening as the local foci of pus formations are removed. 2 

1 Dental Cosmos, May, 1914, p. 568. 

2 Journal of Allied Societies, June, 1914. 



BONE INFECTION ASSOCIATED WITH DENTAL LESIONS 633 

The symptom-complex 1 is mainly an anemic, pasty complexion, 
malaise, loss of appetite, debility, night sweats, loss of weight, low 
fever (100°), or subnormal temperature, which, together with the 
local inflammation (muscles, joints, etc.), should lead to dental 
examination by skiagraphy for obscure conditions as blind apical 
abscess or the investigation of septic conditions under crowns, 
bridges, etc. (as septic gingivitis, septic spaces under crown bands or 
in the cement, gangrenous tooth pulps, pyorrhea alveolaris, fistulse 
leading to chronic abscess, tonsillar or sinus infection. In short, 
any source of sepsis, some of which may require the services of other 
specialists. 

The abscesses are within the bone of the jaw while the dental 
symptoms may not be noticeable though the tooth may be slightly 
tender and there may be tenderness upon pressure over the apical 
region. There may be pain about the eyes or in the back of the head 
or neck. The postcervical glands may be enlarged. The fact 
that teeth have apparently been attended to is no warrant that 
septic conditions are not present, these conditions embracing any 
form of gingivitis or of pericemental infection, including pyorrhea, 
a blind abscess may at any time become acute, and finally establish 
a fistula, sometimes irregularly and without much pain. 



BONE INFECTION ASSOCIATED WITH DENTAL LESIONS. 

During the course of acute and chronic abscess the bone-marrow 
becomes -inflamed by the pyogenic organisms and is broken down 
into pus. The condition may continue after extraction for apical 
abscess in the second stage, or if necrotic bone result in advanced 
pyorrhea. It may also occur from the bruising of the periosteal 
lining of the alveolus as the result of extraction of a hyper- 
cementosed root, or from a bruise induced by forcible use of 
forceps in the removal of deeply seated roots. 

The walls of the alveolus become infected by pyogenic organisms, 
among which the Diplococcus pneumoniae figures prominently. 

The leaving of cotton tampons, placed as vehicles for pain-relieving 
agents, for an undue length of time also invites infection. 

If during extraction the alveolar margins be lacerated, and espe- 
cially if the bone be uncovered by clot, or the clot fail by solution, 
it also becomes infected and ulcerated, as shown by its suppurating 
and highly irritable surface; later the surface becomes insensitive, 

1 Dental Cosmos, May, 1914, p. 569. 



G34 DISEASE OF PERICEMENTUM BEGINNING AT APEX 

indicating superficial necrosis, which may become progressively 
deeper. The clot seems to fail at times after extraction with anes- 
thetics containing adrenalin or suprarenin. In some cases the socket 
may be free of blood for several minutes after extraction. Ragged 
gum margins may become gangrenous, although sometimes not. 
After extraction any loose margin of gum or rough edges of process 
should be trimmed up. 

Symptoms. — The symptoms are those of local inflammation with- 
out necessarily much swelling of contiguous tissues, such as occurs 
in acute abscess. Some circumscribed swelling may occur, indicating 
an abscess in association with it, or a diffuse swelling, indicating 
inflammation of contiguous tissue. The orifice may appear as 
though normal, but close examination demonstrates a sinus leading 
to ulcerated or necrosed bone. If due to an acute abscess in the 
second stage, the symptoms of that condition may continue. As a 
rule, the patient presents within a week of the date of extraction, 
complaining of pain. 

In the majority of cases the pain is of a deep, boring, continuous 
character. Reflex pains are also produced about the face. Much 
debility is caused by the wearing character of the pain, the loss of 
sleep and appetite, and probably also because of absorption of 
toxins. The gum margins are perhaps sloughing; the bone may be 
exposed and exquisitely painful to touch, or it may be necrotic and 
insensitive superficially. The case is one termed "dry socket." 

Cases of general septicemic or pyemic infection from this source 
have been recorded. 

Treatment. — The mouth and, in so far as possible, the inflamed 
part must be sterilized. Probably mercuric chlorid in hydrogen 
dioxid (1 to 1000) will answer best. If the solution be used hot, 
whether it be mercurialized or not, the pain is much relieved. 

An injection of a 1 or 2 per cent, solution of cocain into the healthy 
tissue overlying the alveolus will assist in alleviating the acute pain 
and partly anesthetize the parts. All sloughing gum should be cut 
away. Exposed bone should be anesthetized by strong cocain solu- 
tions if painful to touch, or the patient should be anesthetized if 
necessary. Whether acutely inflamed or necrotic, the bone should 
be cut away with large sterile burs until healthy tissue is reached. 
After washing out the debris and further sterilization a clot is to 
be induced by curetting if necessary. The mouth is to be kept 
sterilized and, the patient is to be seen daily for a repetition of the 
curetting if the clot fail, or the alveolus may be gently packed with 
cotton saturated with balsam of Peru alone or with castor oil, equal 
parts, as a stimulant. In ordinary cases one or two local treatments 



EXTENSIVE NECROSIS (535 

will be effective, but the tonic, antiseptic, systemic medication 
recommended under the heading of acute apical abscess is advised. 

As a stimulant for granulating sockets, tincture of iodine diluted 
with equal parts of tincture of aconite or alcohol is valuable because 
of its irritant and disinfectant qualities. The socket is wiped with 
it daily. 

If the infection be of aggravated character, precautions in the form 
of suitable systemic medication should be taken against a possible 
septicemia. (See p. 604.) 

If the patient be not willing, or is unable, to bear this operation at 
the first visit because of the demoralization produced by the pain, 
an alternative proceeding may be adopted. A pellet of cotton wet 
with campho-phenique should be rolled in powdered orthoform and 
introduced into the socket after sterilization with iodine, or a stiff 
mass made from orthoform, zinc oxid, and vaselin may be packed 
into the alveolus as an antiseptic and anesthethic. (Jack. 1 ) Tri- 
chloracetic acid in saturated solution, or silver nitrate, or aromatic 
sulphuric acid may be used as a special stimulant and the balsam 
packing renewed. The repetition of this after five to eight hours 
will afford marked relief. Later the radical operation may be per- 
formed if granulation does not set in. The introduction of cotton 
or gauze dressings into the alveoli for relief of pain immediately 
following extraction is to be done only with extreme care and for 
short periods, as such dressings are apt to be left in place by 
patients, and, becoming septic, act as causes of sepsis of the alveolar 
process. It is better to induce a clot if the removal of the cotton 
is not followed by hemorrhage. While alveoli will fill with granula- 
tions in the absence of a clot filling them, such a clot seems to be 
the best protection against sepsis and a depressed scar tissue. In 
some of these cases portions of bone may exfoliate. In one obsti- 
nate case the capsule of bone surrounding the apex of the alveolus 
came away. 



EXTENSIVE NECROSIS ASSOCIATED WITH CHRONIC 
ALVEOLODENTAL ABSCESS. 

The illustration (Fig. 585) is that of a case of necrosis with two 
external pus sinuses along the lower border of the mandible, associated 
with great pain on recumbency, rise and fall of body temperature, 
and occurrence of stupor and coma. The operation consisted of ex- 

1 International Dental Journal, 1905. 



636 DISEASE OF PERICEMENTUM BEGINNING AT APEX 

traction of the cuspid and first bicuspid, removal of the sequestrum, 
curettement of bone, and drainage. 1 

Fig. 585 




The white line is artificial and shows the extent of the sequestrum (see text). 
(Skiagraph by Raper.) 



Every chronic alveolodental abscess carries with it the danger of 
bone complication. It has been shown that in bone infection the 
organisms are highly virulent. Fortunately in most cases the involve- 
ment is slight and the parts care for themselves when the cause is 
removed. In more aggravated cases, either caries or necrosis of the 
bone may follow. Pus is formed at the expense of the parts, and 
sometimes infiltrates the surrounding soft and the hard parts, caus- 
ing the loosening of teeth. This may occur even though the causal 
tooth be extracted. In caries the pus escapes by several fistula? 
and examination leads to porous dead bone. In necrosis there 
is circumvallation of a portion or portions of bone, and finally one 
or more sequestra are loosened, and later, in part, liquefied. The 
remainder gradually works out of the fistula as one large or numerous 
small pieces. The patient may be much debilitated. In syphilitic 
or strumous cases an otherwise simple case may positively refuse 
to heal until the physical condition is improved by antisyphilitic 

1 Practice of Dr. Gilmer, description by Howard R. Raper, Items of Interest, July, 
1912. 



SEPTIC PERFORATION 637 

or tonic treatment. Surprising recoveries of extensively necrotic 
parts occur if the patient be brought into good physical condition, 
and the parts are antiseptically treated, the thorough loosening of 
the sequestra being awaited. By this means teeth have been retained 
in place and covered with new tissue, which operation would have 
exposed or removed. The determination of the point at which oper- 
ative interference is desirable must depend upon the particular 
case and the amount of deformity likely to result from the operation. 
In some marked cases with toxemia, drainage must be obtained 
surgically, even if extreme operation be necessary. 

Honl and Bukovsky are credited with the successful treatment 
of bad chronic suppurations by means of local applications of 
py ocy aneoprotein . 

Jensesky 1 so treated a case of six months' standing, incurable by 
ordinary antiseptic and systemic treatment, and obtained remarkable 
results. Vaccine therapy is also useful. 

Syphilitic intoxication or that of scarlet fever may cause a necrosis 
of alveolar bone, as may mercury. (See p. 231.) The extent to 
which the teeth or oral infection act as active exciting causes depends 
upon the condition present. 

SEPTIC APICAL PERICEMENTITIS COMPLICATED BY 
PERFORATION. 

In the treatment of root canals the required mechanical work 
sometimes results in (1) the passage of the drill through the apical 
foramen,, enlarging it; (2) through the side of the root, causing a 
perforation. 

In the first variety the complication chiefly concerns the root 
filling, which is to be conducted after sterilization upon the same 
plan as for filling an incomplete foramen. (See p. 555.) 

If a lateral perforation be made near the root apex, it may be 
filled after sterilization with a cone similarly applied, but made 
bevelled at the end, or a bit of aseptic sponge may be introduced 
against the tissue for a base and be covered by oxychlorid of zinc. 
The packing of a fairly stiff mass of zinc oxychlorid into the root 
and through the perforation into the fistula has caused the healing 
of several obstinate cases continually weeping pus or serum. The 
moisture, if slight, rather aids the adaptation of the cement. The 
same treatment used with greater care is useful in chronic abscesses 
without fistula. It is well to fill only the apical portions of canals in 

1 Dental Cosmos, 1901. 



638 DISEASE OF PERICEMENTUM BEGINNING AT APEX 

either case, so that any removal for another trial may not be too 
difficult; the later filling of the coronal portion of the canal is very 
simple. The use of a stiff paste of zinc oxid and eugenol or even 
oxyphosphate of copper in the same manner is useful. If possible, 
it is well to irrigate the fistula with water to remove any excess, 
though if left it usually works out of the fistula, which later heals 
or not, as the case may be. If septic conditions persist, the root 
end must be amputated, or the tooth extracted, prepared, and 
replanted. If made in the middle third of the root, the canal must 
be sought for and treated as usual beyond the perforation, which is 
then separately treated with a gutta-percha cone, or a plaque of 
gutta-percha may be laid over the perforation and antiseptic cements 
or copper amalgam used to secure it in position. Extraction and 
replantation may be resorted to, but amputation does not serve 
so well, as the root leverage is lost and the tooth may loosen. In a 



Fig. 586 



t 



Fig. 587 



Skiagraph of crowned curved root, with 
perforation and protruding root filling 
near apical foramen. With septic con- 
ditions, would require root amputation, 
(Price. 1 ) 




Showing the relations of an abscess 
upon a temporary tooth, with the crown 
of a developing permanent tooth under- 
lying it. 



favorable case, after canal exploration, a tapering probe may be 
passed into the canal and copper amalgam gently tamped about it 
and against the perforation; the probe is then withdrawn, leaving 
a central canal, which is later treated. Gird wood has reported good 
results from the use of copper amalgam, which, in this connection, 
the writer can confirm. In a few cases the fistula has been packed 
open and the perforation filled with amalgam through the sinus. 
The cases are mostly successful, but in one case healing did not 
occur until treatment after filling was suspended for several months. 
Chronic Septic Pericementitis in the Temporary Teeth. — Any of the 
chronic septic conditions described may occur upon the temporary 
teeth. The presence of resorption and of the permanent crown 



Items of Interest, 1901. 



APICAL PERICEMENTITIS IN TEMPORARY TEETH 639 

usually confines the inflammation to a point lower in the alveolar 
process than in the case of permanent teeth. The loose character 
of the structure causes the ulceration to occupy a larger area, and 
the parts in chronic inflammation look more angry, but are fairly 
well tolerated. The treatment is practically the same for the curable 
cases; the others should be extracted. The root canals when treated 
should be filled with absorbable materials, such as paraffin or wax 
combined with aristol. Buckley recommends, as a canal filling in 
these cases, the use of a stiff mixture of calcium phosphate and 
formocresol (formalin, 1 part; cresol, 1 or 2 parts), to be packed into 
the pulp chamber and zinc phosphate quickly flowed over it; the 
cavity to be filled later. 

Johnson 1 suggests that a eucalyptol solution of gutta-percha (see 
p. 551) be pumped into the canals and pressure exerted with tempo- 
rary stopping until the solution appears at the fistula. The tem- 
porary stopping that does not interfere v%ith filling integrity should 
be left. 

Chronic Septic Apical Pericementitis (Non-purulent). — Continued 
apical inflammation of a low grade probably is a condition analogous 
to blind chronic apical abscess or the infection leading thereto. 

Cause and Pathology. — The cause consists of unremoved gan- 
grenous pulp tissue, septic serous collections in canal apices or 
about imperfect root fillings, or septic material in the root tubuli, 
all much the same in character. A very common cause is an other- 
wise good root filling which has failed to fill the apical portion of a 
curved fine or even well-opened root. While in skilful hands gutta- 
percha points and oxychlorid of zinc usually reach their apical 
destination, the editor has met unfilled apical canals after good 
operators as the most common of operative errors. 

An imperfectly filled perforation may cause a similar condition, 
which, however, the .r-rays should determine. 

Albuminous fluid may enter the canal via the apical foramen, and, 
becoming infected, putrefaction ensues. The source of infection 
may possibly be via the blood, but leaking crown and root fillings 
more probably permit bacteria to enter from the mouth. The 
more or less constant result of filling roots with cotton permeated 
with evanescent materials only is evidence of this. The cotton 
absorbs fluid either from about leaky fillings, too often placed in 
contact with it, or else from the apical tissues; infection readily 
occ,urs and a highly odorous cotton is removed because of the apical 
irritation. When the cotton is well placed and confined under 

1 Dental Cosmos, 1899. 



640 DISEASE OF PERICEMENTUM BEGINNING AT APEX 

tight-sealing materials to the apical half of the root canal, this 
result is long delayed in many cases. Portions of gangrenous pulps 



Fig. 588 



Fig, 589 



Sector of a cross-section from a dis- 
eased root: a, cementum; b, stratum 
granulosum; c, very narrow and finely 
branched tubules; d, penetration of 
bacteria into tubules. X 150. 
(Miller.) 




Dentin from the root of an abscessed 
tooth, showing the penetration of cocci to 
a depth of about T V mm. (2I0 m ! the 
side a to 6 bordered upon the canal. 
X 1000. (Miller.) 

remaining in canals may likewise 
become infected. Extra and un- 
treated canals are frequently causes. 

Miller 1 has shown that root 
tubules are infected only for a 
short distance at their canal ends, 
so that infection from the perice- 
mentum via the cementum and 
dentinal tubules is highly improb- 
able (Fig. 559). The putrefaction 
produces gases, and these exuding 
slowly produce the irritation. If 
pyogenic organisms be present, 
apical abscess may at any time 
supervene. 

Mayrhofer 2 has shown that even 
formocresol fails to sterilize all 



1 Dental Cosmos, 1899. 



2 Items of Interest, March, 1910. 



CHRONIC SEPTIC NON-PURULENT PERICEMENTITIS 641 

tubuli, so that bacteria, especially streptococci, grow back into the 
canal. If the canal filling be imperfect it is obvious that apical 
infection may arise. 

Symptoms. — Subacute inflammation of apical tissue being present, 
the symptoms of this condition are tenderness upon decided pressure 
or upon percussion; the response may only be elicited by pressure 
or percussion in one direction. The tooth gives a dull note upon 
percussion, and is usually looser than its neighbors. The red line of 
the gum extends farther toward the gum margin than normal — quite 
to it in some cases. There is apt to be a response to heat. 

The patient is apt to avoid the tooth in mastication. In some 
cases acute reflex pains in other teeth may precede an outbreak of 
acute purulent pericementitis, a frequent sequel to this condition. 
There are also evidences of previous devitalization of the pulp in 
opacity, lack of response to tests for vitality, etc. At times a history 
of previous canal treatment may be obtained or the evidences of an 
attempt at canal filling may be seen upon opening the tooth. The 
systemic symptoms if any are those mentioned under chronic apical 
abscess. 

Diagnosis. — The condition requires careful differentiation from (1) 
non-septic apical pericementitis due to traumatism or malocclusion 
or to a perforation imperfectly filled; (2) pericemental abscess in 
the early stage; (3) abscess of the pulp in the later stages. In nearly 
all these cases the pulp may be vital. Being itself only subsequent 
to death of the pulp, tests for vitality are made. (See p. 563.) 
If pulp death be indicated by the tests, the pulp canal is explored, 
and, if found, treated and filled; a septic condition about or beyond 
the same is looked for. 

There is great disadvantage in a large apical opening, particularly 
in the dressing and root-filling operation. 

Treatment. — The condition being analogous to that of moist 
gangrene, or blind apical abscess, the treatment is the same. Before 
it can be applied the root canals should be opened, and to accomplish 
this all root fillings involved require removal. If an extra canal be 
found after apparently conscientious work has been done, this 
should receive attention before removing root fillings. 

The bulk of gutta-percha root fillings are best drilled out with 
Downie broaches revolved in the engine hand-piece or by hand, 
eucalyptol being used to soften or dissolve the gutta-percha. 

All cement fillings are removed by a drill so far as can be safely 

done, dryness being a great aid in locating the cement in the canal. 

When the danger of perforation arises, a stiff Swiss broach or a fine 

Downie broach may be rubbed down to a drill edge and used as a 

41 



642 DISEASE OF PERICEMENTUM BEGINNING AT APEX 

tamp drill. Sulphuric acid in 50 per cent, solution or aqua ammonia 
aid by dissolving the cement. 

The object sought for is an unfilled canal lumen, which, when 
found, is readily recognized by the ease of penetration with the 
broach and the absence of sensation until the apical tissue is reached. 
The fact that the sides of the root canal can be felt is assurance of 
safety against perforation which may occur in any case. 

There can be no assurance of safety until the apical tissue can be 
explored, but perforation must be avoided. The fine Downie broach 
is useful in difficult cases, and, if necessary, a No. 1 Beutelrock drill 
may be used. When the apical foramen is open, or further work is 
impossible without the danger of perforation, the canal treatment is 
conducted upon the lines laid down for gangrenous pulp. (See p. 
579.) A difficult class of cases sometimes presents in which the 
disease supervenes and where work which may be regarded as des- 
perate has been done, or where pins have been inserted and are 
almost impossible of removal, as, for example, where a Logan crown, 
has been cemented to place. In such cases the idea of Watkins in 
applying blue light directly by means of a funnel may be of great 
value in reducing inflammation, and mild applications of the arrays 
or the high-frequency violet ray may be useful, but sometimes the 
work must be carefully dismantled to permit retreatment. An axray 
should always be first made as a guide. 

If the pericementitis have been of long standing, the thickening 
of the membrane will have caused protrusion of the tooth. The 
tooth should be ground off at its point of occlusion until it occludes 
with somewhat less force than its neighbors, the therapeutic principle 
in these cases being that of removing the source of irritation and 
procuring surgical rest. Indications of favorable results are found 
in the red gum line assuming its normal position, tenderness disap- 
pearing, and increased tightness of the tooth. 

This affection is extremely common about the roots of pulpless 
teeth, and always signifies more or less enforced disuse of the teeth, 
and, if uncorrected, their ultimate loss. 

This condition is sometimes associated with a chronic blind abscess. 
(See p. 631.) Upon treatment, acute apical abscess is apt to be 
lighted up; therefore the sterilization should be prolonged and 
thorough to avoid acute apical abscess. In one case of a cyst asso- 
ciated with a lower molar tooth which had a leaky gutta-percha 
crown and partial canal filling, extraction was advised for reasons 
other than canal treatment. The cyst then promptly developed as 
an acute abscess, which shifted its position toward the cheek and 
there discharged without production of scar. 



SEPTIC PERICEMENTITIS AT BIFURCATIONS 643 

Septic Pericementitis at Bifurcations of Multi-rooted Teeth. — 

Teeth weakened by caries may fracture after filling in such a manner 
that the line of fracture exposes the pericementum at the bifurcation. 
The crack admits septic saliva, and a filling or fillings usually sink 
gingivally, wedging apart the two sections and admitting more or 
less food matter. If the canals of the sections have been previously 
treated and filled, it is usual to find a more or less general peri- 
cementitis due to the wedging and septic irritation. It subsides upon 
sterilizing by means of a douche, while gentle broaching removes the 
accumulated debris. Formocresol, diluted with phenol camphor to 
a 5 or 10 per cent, formalin strength, is to be placed in the pulp 
cavity and covered with sandarached cotton, and a ligature of silk 
or wire is to be tied about the tooth to draw the parts together. A 
hollow metal crown is to be constructed and before placement a 
little oxyphosphate of copper or oxychlorid of zinc cement is to 
be worked into the joint, which is temporarily sprung open. The 
part may be joined by amalgam built into a dove-tail (Fig. 312), 
or a trephine may be driven into the face of the crown and a metal 
ring be cemented into it (Fig. 316). 

If the canals be septic, an apical abscess may complicate the 
condition and require treatment while the fracture is being handled. 
In some cases a metal staple may be placed in the canals of the two 
sections and so arranged as to spring the parts together when forced 
to place. The joint should have one of the cements worked into it 
before this staple is cemented to place. About the staple quick- 
setting amalgam should be packed, a copper band having been pre- 
viously adjusted to act as a matrix. Later, this band is to be removed 
and a porcelain-faced gold crown or a porcelain crown baked on a 
heavy wide platinum band and cap arranged to sustain it (Fig. 294). 

The staple may be utilized as a portion of a crown base of the 
Richmond or other variety, the bifurcation and crown cementing 
being deferred until the final operation. Irritation may arise in 
some of these cases, which, however, need not prevent the trial of 
the method as a last resort. 

The methods of tooth salvation here indicated are subject always 
to the general principle of extraction when advisable. In no case 
should teeth in inoperable condition be saved at the expense of the 
individual through constant pus formation. 



CHAPTER XXL 
NON-SEPTIC PERICEMENTITIS. 

Various grades of pericemental irritation, ranging from a mild 
arterial hyperemia to actual inflammation, may be produced by 
non-septic causes. 

The most satisfactory evidence that inflammation may be so 
caused is furnished by Talbot's experiments with the mercurialization 
of dogs. Beginning with healthy pericementi, these were, after 
mercuiialization of the animal, found to contain the round-celled 
infiltration characteristic of inflammation, and no bacteria could be 
found. Further evidence is given by the usual experimental study 
of inflammation with the mesentery of the frog. Simple irritation, 
even with antiseptic substances, produces the phenomena. Any of 
the causes which may produce inflammation may, if acting in more 
mild degree, produce arterial hyperemia. If the action of the cause 
be violent and then discontinued, as in the case of a blow, the inflam- 
mation resulting is acute, but may pass into a chronic form; but if 
the cause continue to act it produces a chronic inflammation. 

For purposes of description, non-septic pericementitis may be 
divided, according to its character, into traumatic and symptomatic, 
and, according to its location, into apical and general. 



TRAUMATIC PERICEMENTITIS. 

By traumatic pericementitis is meant a profound irritation of the 
pericementum, the result of mechanical violence applied externally 
to the tooth, or of instrumentation or chemical irritation of the 
pericementum through the root canal. 

Causes. — Violence Externally Applied. — Excessive force deliv- 
ered directly upon the teeth, as in case of" blows, falls, overmalleting 
in building fillings, the biting of nuts, thread, or other hard objects, 
or force indirectly delivered, as in case of blows received under the 
chin, bringing the teeth forcibly together, may all cause acute peri- 
cementitis. 

An excessive amount of filling on the occlusal surface of a tooth, 
a maloccluding crown or overful fillings upon the proximal aspect, 
(644) 



TRAUMATIC PERICEMENTITIS 645 

maintaining a wedged condition, cause overocclusion upon the tooth 
and an irritation of its pericementum. 

The overstraining of the pericementum of a tooth as the result of 
overuse, as in cases where only a few teeth remain for mastication, or 
where pyorrhea or calculus has caused resorption of the alveolar 
process and looseness of the teeth, or where artificial dentures are 
clasped to remaining teeth, or where bridges are supported upon 
insufficient piers, are frequent causes of non-septic pericementitis of 
a degenerative character. The presence of a rough flaring or a too 
deeply placed crown band beneath the gum margins, portions of 
cement used in cementation of crowns, or excess of filling material 
beneath the gum, are all causes of marginal gingivitis, with which 
pericementitis may be associated. With these marginal cases septic 
causes usually have to be considered as complications. 

Too violent wedging is always followed by more or less peri- 
cementitis of the wedged teeth, and their neighbors, more marked 
when elastic-rubber wedges are used. 

In correcting irregularities of the teeth, if they be moved too 
rapidly, are not firmly directed during the operation, or, subse- 
quently, not firmly maintained in position, pericementitis of a high 
grade is frequently excited. (See Overuse and Malocclusion of Teeth.) 

Violence Internally Applied. — If a wholly or partially vital 
pulp be torn from its apical connections, as in the use of pressure 
anesthesia, an apical traumatic pericementitis may be set up. This 
is usually transient. Secondary hemorrhage may occur and produce 
pericementitis. 

Excessive laceration of the apical tissue by means of barbed 
instruments, the inclusion of air or medicament under a root dress- 
ing or filling, the same exercising pressure upon the apical tissues; 
the mechanical irritation of a projecting root filling, pivot wire, 
broach, or drill, are all sufficient causes. 

The undue enlargement of the apex of the root canal or the passage 
of a reamer through the lateral aspect of a root may excite inflam- 
mation, and the perfect filling of the opening may be exceedingly 
difficult, so that if the tissues are not infected at the time, sepsis 
may later follow. 

Chemical Irritation. — The application of arsenic to a perfora- 
tion may excite inflammation and necrosis, which endangers the 
jaw. (See p. 528.) The use of arsenic as a pulp devitalizer may 
cause a hyperemia of the apical tissue, following the hyperemia of 
the pulp, and causing slight tooth extrusion, which is aggravated 
by the malocclusion. This is not dangerous. (See p. 521.) 

The undue use of escharotics, such as carbolic acid, sodium dioxid, 



646 NON-SEPTIC PERICEMENTITIS 

zinc chlorid, sulphuric acid, or mercuric chlorid, in a pulp canal 
may excite an undesirable irritation. The limited irritation follow- 
ing their limited use is often more than offset by the advantages of 
the asepsis produced. 

Prophylaxis. — Many of these causes are avoidable, and operators 
mindful of possible irritations should avoid the mechanical irritation 
of apical tissues, neutralize powerful acids or alkalies, use escharotics 
with caution, wedge teeth gradually, and after wedging either pack 
gutta-percha between the teeth to permit them to rest for a few 
days or fix them immovably with wooden wedges or steel separators 
during malleting. 

During orthodontia teeth should be moved steadily, and after 
alignment is secured they should be firmly maintained in position 
until deposition of bone occurs. 

Patients should be warned against the evil effects of thread biting 
and biting hard substances. 

Pathology and Morbid Anatomy. — Chemical substances applied in 
excess cause a destruction of tissue dependent upon the quantity 
used. Inflammation tending to the resorption of the dead tissue 
occurs. The pericementitis presumably persists in some degree 
until the foreign (dead) material is removed by natural processes. 

In the case of protruding foreign bodies, such as root fillings, 
broaches, etc., there is a tendency of the inflammation to become 
subacute or chronic. The foreign body may to an extent become 
encysted, particularly in the case of a gutta-percha root filling. In 
other cases the continued vascular disturbance, if of mild degree, 
produces hypercementosis; in more severe cases resorption of the 
root occurs. 

Cases due to perforation of the root and wounding of the peri- 
cementum, after the acute symptoms have passed, commonly assume 
an irritative and chronic type, the soft tissues included in the per- 
foration being in a state of chronic inflammation. Many of these 
cases become infected owing to the difficulty of completely sterilizing 
the apical portion of the canal which lies beyond them. 

The pericementitis produced by pressure of included air, liquid, 
or plastic root filling upon the apical tissue is often severe. Upon 
removal of the root dressing or filling the engorgement is relieved 
by the gushing of blood through the root canal. The inflammation 
may, however, continue unless sedatives be applied to the apical 
tissue via the canal. 

In cases due to traumatism, such as violent wedging, rapid move- 
ment in regulating, overmalleting, blows, biting of thread, ice, nuts, 
etc., the condition is surgically one of bruise. 



TRAUMA TIC PERICEMENTITIS 647 

The phenomena of active inflammation make their appearance to 
an extent governed by the degree of violence — exudation, swelling, 
redness, and pain; fibrinous and corpuscular exudations occur, and 
later a reorganization of tissue occurs, in some cases a degeneration, 
depending upon the completeness with which the indicated thera- 
peusis is applied and upon the vitality of the pateint. 

Traumatic pericementitis in high degree in the young may be 
recovered from : but in the middle aged and aged it may give rise to 
a series of degenerative changes which end only with the loss of the 
tooth. 

In cases due to looseness of the teeth, of course, septic primary 
causes have to be considered, but the pericementitis may be quite 
as much mechanically as septically produced. 

In all cases the extrusion caused by the inflammation adds another 
exciting cause of apical pericementitis — i. e., malocclusion, which 
aggravates the condition. 

Symptoms and Diagnosis. — The amount of pericemental inflamma- 
tion present is evidenced by the soreness and extrusion of the tooth 
and the degree of redness in the overlying gum tissue. 

A history of violence may be obtained when it has occurred. Mal- 
occlusion may be detected by occlusion marks upon fillings or by 
means of carbon paper. The untoward results of canal operations 
may be inferred from a personal knowledge of the case or, perhaps, 
from the history. It is at times difficult to exclude septic, non- 
purulent, apical pericementitis as a cause, particularly if the case 
come from the hands of another practitioner. In doubtful cases 
the treatment for inferred traumatisms may be employed, and if 
followed by good results a post hoc diagnosis of traumatic peri- 
cementitis may be made. The .r-rays afford a means of determining 
extruding root fillings, broaches, etc. 

Treatment. — Foreign bodies protruding from the root apex must 
be removed if persistent symptoms demand it. This may require 
an artificial opening for its performance, or root amputation. Per- 
forations should be carefully treated. 

If evidence of pericementitis persist, the end of the root including 
the perforation should be amputated, or if the tooth persistently 
extrude, the tooth may be extracted, the perforation and canal filled 
with gold or gutta-percha, and the tooth replanted under antiseptic 
precautions. 

In all cases due to violence the treatment is that adapted to injury; 
first, surgical rest of the pericementum. This may be accomplished 
in two ways: either by preventing the tooth striking its antagonists 
or holding it so rigidly that it cannot move if it does meet them. 



648 NON-SEPTIC PERICEMENTITIS 

As a preliminary measure the tooth is gently but firmly lashed 
to its neighbors by means of ligatures so that it is rigidly held. A 
swaged cap is either fitted to a neighboring tooth, or the antagon- 
izing teeth are ground away until they fail to strike the injured 
tooth; the first method is to be preferred. 

In cases involving several teeth, such as all of the incisors, two 
metallic plates are quickly swaged to cover posterior teeth and raise 
the bite, and they are cemented in position to relieve the irritated 
teeth from occlusion. 

When the apical tissues have been irritated by way of the canal, 
sedatives, such as strong tincture of aconite or menthol in chloroform 
phenol-camphor, eugenol, or menthol-phenol 1 (menthol, 3 parts; 
carbolic acid, 1 part; melted together) or thymophen should be 
applied on cotton to the apical tissue by way of the root canal. All 
cases of traumatic pericementitis require the persistent use of counter- 
irritants, applied every other day to the overlying gum. (See p. 476.) 

Systemic derivation is also useful in the acute cases. In even 
mild cases not due to violence the guarding of the extruded tooth 
against malocclusion is of advantage. 

If the cause be some mechanical irritant at the gum margin, this 
should be removed and the case treated as above described. Recog- 
nizing the possible influence of septic causes, oral antiseptics are to 
be used. 

SYMPTOMATIC NON-SEPTIC PERICEMENTITIS. 

By symptomatic non-septic pericementitis is meant an aseptic 
pericementitis occurring as the result of systemic conditions, or of 
the action of drugs taken internally. 

If mercury be administered to patients in large doses for long 
periods, or in one or more massive doses, or if the patient have an 
idiosyncrasy to the action of this agent, or be a worker in mercurials, 
an irritation of the salivary glands is excited, followed by looseness 
and soreness of the teeth and swelling of the gums; that is, a general 
pericementitis and maxillary periostitis arise. The patient has a 
metallic coppery taste, coated tongue, and fetid breath; the gums 
are puffy and bleed easily. In advanced cases the tongue and cheeks 
are swollen. Potassium iodid administered in this condition relieves 
the maxillary periostitis and pericementitis; but the same drug 
administered in health, or for conditions other than mercurial 
poisoning, also causes irritation of the pericementum. Pilocarpin 

1 Dr. Morgan Howe, 



SYMPTOMATIC NON-SEPTIC PERICEMENTITIS 649 

has a similar effect, though in much less degree. All of these drugs 
are partially eliminated by the glandular appendages of the mouth, 
and during elimination apparently act as local irritants. Lead 
poisoning may have a similar action. A blue line appearing on the 
gums is symptomatic. It occurs in painters and workers in lead. 
Lead has been found in the calculus on the teeth and even in the 
tooth substance. 

Patients who have a gouty heredity, or who are the subjects of 
active gout, frequently exhibit a tenderness of the entire pericemen- 
tum of one or more or sometimes all of the teeth. This pericemental 
disturbance may be the precursor of an acute outbreak of gout in 
the metatarsophalangeal joint. 

Scurvy — a very rare systemic disease — is attended by rapid 
degeneration of the pericementum of the teeth and of the alveolar 
tissues. 

Syphilis is also attended by pericemental irritation. This, of 
course, is of septic origin. 

Talbot's experiments on dogs show conclusively that a true peri- 
cementitis may be induced owing to the chemotactic properties of 
the mercury alone. (See Interstitial Gingivitis.) 

In auto-intoxication by intestinal toxins or by leukomains in 
diseases involving general malnutrition, the irritants are probably 
in part eliminated by the gums, which are in turn irritated. (See 
Pyorrhoea Alveolaris.) 

It has been shown by Loup that mercurial stomatitis may be 
cured by mercury used as an oral antiseptic; therefore, the logical 
conclusion is that oral organisms play a part in the production of 
the local effects of mercury; probably the mercury produces a local 
predisposition. This is further confirmed by the fact that if the 
teeth are attended to and oral prophylaxis be practised before the 
administration of mercury to syphilitics, they tolerate greater 
amounts of the drug before salivation or stomatitis. 

Treatment. — The drug should be discontinued, the disease, if 
present, should be antagonized, and the local complications, if any, 
should be appropriately treated, antisepsis being always advisable. 
If the pericementitis, gingivitis, and stomatitis be mercurial, the 
drug should be stopped and an antisialagogue used, such as atropin 
sulphate, r ^ gr. each four to six hours, until relieved. 

Potassium chlorate as a mouth wash, or internally, is useful if the 
stomach is not irritable. 

1$ — Potassii chloratis gr. xlviij 

Tr. myrrhse f 5ss 

Elixir calisayae q. s. ad fgiij — M. 

Sig. — Teaspoonful every five hours, or use as a mouth wash. (Hare.) 



650 NON-SEPTIC PERICEMENTITIS 

Results of Chronic Non-septic Pericementitis. — If at any point of 
the irritated pericementum a constructive grade of irritation be 
maintained, the cemental tissue becomes hypertrophied (Fig. 590). 
If a more severe grade of irritation — i. e., low-grade inflammation 
— be present for a long time, the cementum and even the dentin 
of the root may be resorbed. Both of these results may go on 
concurrently at different points, or resorption may be followed by 
deposition of cementum if the conditions change. 

Chronic overuse or disuse of teeth results in degenerations of the 
pericementum. (See p. 661.) 

HYPERCEMENTOSIS (DENTAL EXOSTOSIS, EXCEMENTOSIS, 
HYPERPLASIA OF THE CEMENTUM). 

Definition. — By hypercementosis is meant a secondary deposit, or 
an increase of volume of the cementum of a tooth beyond the normal 
limit. It may be circumscribed or diffuse. 

Causes. — A constructive degree of hyperemia or very mild inflam- 
mation is the proximate cause, which may be excited by numerous 
primary causes, such as a projecting root filling, a projecting edge of 
crown filling, deposist of salivary calculus, the overlapping of a cavity 
margin by the gum, malocclusion, non-occlusion, the biting of hard 
objects, such as nuts or thread, the overuse of certain teeth, the 
habitual tapping together of teeth, the habitual chewing of tooth- 
picks, the gradual pressure of gas from dead pulps. The pressure of a 

Fig. 590 







tooth root against another root during eruption is a sufficient cause. 
(See Fig. 173.) The overcrowding of teeth in an arch has also 
caused this condition, as has also the impaction of a tooth (Fig. 218). 
Chronic alveolar abscess or pyorrhea alveolaris may cause it by 
inducing about itself at a distance an area of hyperemia. (Aseptic 
Area.) It also seems at times to be induced after pulp devitalization 
from any cause. Hypercementosis is a possibility in any case of 
chronic pericemental irritation; it represents a degree of irritation 



HYPERCEMENTOSIS 



G51 



rather than any one specific cause. It has been discussed by some 
writers under the heading of Constructive or Condensing Perice- 
mentitis, and is fairly analogous to osteosclerosis. (See p. 144.) 



Fig. 591 




Hyperoementosis. (Skiagraph by Lodge.) 

Situation. — Hypercementosis may be diffused over almost an 
entire root or several roots, or be localized as a distinct nodule at 
some lateral aspect, or exist as a circumscribed enlargement about 
the apex of a root, or at the neck of a root. It is always located 
where the cause (hyperemia) has been produced (Fig. 590). 

Fig. 592 



r'S :Z y::\ 



Y//M 



IS 



Wm 



Hypertrophy of the cementum on the side of a root of a lower molar near the neck 
of the tooth of a man: a, dentin; b, cementum; c, fibers of peridental membrane; 
from b to c the cementum is normal and the incremental lines fairly regular, but at 
d one of the lamellae is greatly thickened; at e this lamella is seen to be about equal 
in thickness with the others. The next two lamellae are thin over the greatest prom- 
inence, but one is much thickened at g, and both at h. These latter seem to partially 
fill the valleys which were occasioned by the first irregular growth. From a length- 
wise section. (Black.) 



Flagg noted that 75 per cent, of cases of hypercementosis were 
found upon posterior teeth, and that the teeth were usually of the 
character termed dense — i. e., the tissues of the individual were of 
recuperative type, tending to produce constructive changes. 



652 



NON-SEPTIC PERICEMENTITIS 



Pathology and Morbid Anatomy. — For some time after eruption 
the cementum consists of but few lamellae of deposit. It, however, 
reaches a maximum normal development at which it normally rests, 
as in the case of the physiological pulp cavity. As age progresses 
it is apt to be more thickly deposited at the expense of the peri- 
cementum, which becomes more attenuated. Whether this is due to 
irritants floating in the blood stream, or to the various local irritants 
above mentioned, or to perfectly normal development, is not clear 
except for certain definite cases. 

Nodular and irregular forms arising from the general surface are 
clearly of abnormal type. 

Fig. 593 




Apex of root of an upper bicuspid tooth with irregularly developed cementum: 
a, a, dentin; b, b, pulp canals. The lamellae of cementum are marked 1, 2, 3, etc.; 
d, d, d, absorption areas that have been refilled with cementum. It will be seen that 
the apices of the roots were originally separate, but became fused with the deposit 
of the second lamella of cementum, and that in this regular growth began and was 
most pronounced. It has continued through the subsequent lamellae but in less degree. 
It will also be noticed that the absorption areas, d, d, d, have proceeded from certain 
lamellae. That between the roots has broken through the first lamella and pene- 
trated the dentin, and has been filled with the deposit of a second lamella. Other 
of the absorptions have proceeded from lamellae which can be readily made out. The 
small points, e, seem to have been filled with the deposit of the last layer of cementum, 
while others have one, two, or more layers covering them. (Black.) 



Successive lamellse are deposited; the pericementum recedes, 
causing resoprtion of the alveolar process. Union of the bone and 
cementum (ankylosis) very rarely occurs. A resorption of cementum 
and dentin may occur at some point owing to a different degree of 



HYPERCEMENTOSIS 653 

irritation, and in the area a new deposition of cementum may occur 
(Fig. 593, d). In some cases distinct areas of hypercementosis and 
root resorption are seen in close proximity. Chronic apical abscess 
may produce a denudation of the root end, and a short distance 
below an annular ridge of hypercementosis may occur. Areas of 
hypercementosis may be translucent or decidedly opaque, and 
sometimes the two are combined, a mottled appearance being pro- 
duced. 

If the growth proximate another root, the pericementum may 
resorb at the point of contact and a deposition of cementum occur 
which firmly unites the roots in a union called concrescence. (See 
p. 263.) 

It has occurred that a root filling protruding through a perforation 
has caused a diffused exostosis of the alveolar process. 1 The hyper- 
trophied process may be ivory-like in hardness. 

Symptoms and Diagnosis. — Many cases exist without active local 
symptoms. In no case is the color of the gum altered unless other 
disease than hyperemia be acting as a cause. In some cases there 
are symptoms of hyperemia expressed as a disposition to bite hard 
upon the particular tooth, or to grind upon it. A paroxysm of gnaw- 
ing pain lasting for some hours, and recurring at intervals, is also 
somewhat characteristic. Sympathetic hyperemia of the pulp with 
increased response to thermal changes may occur. (See p. 469.) 
The gum may have slightly receded. 

Neuralgia, functional blindness, functional deafness, chorea, 
epileptiform fits, paralysis, cardiac neuralgia, insanity, and other 
related conditions have been cured by the extraction of hyper- 
cementosed teeth. 2 

The treatment of teeth presenting obstinate symptoms of peri- 
cementitis, apparently due to moist gangrene of the pulp, may at 
times be complicated by unsuspected hypercementosis. 

In such cases, if pulp or pericemental complication cannot be 
determined, suspicion should point to hypercementosis and an away 
examination be made, by which means the condition may be posi- 
tively determined. As entire dentures have been extracted, tooth 
by tooth, in a vain endeavor to cure a neuralgia about the head, 
this means of diagnosis should not be overlooked. 

Treatment. — The treatment for hypercementosis may first be a 
conservative one if only slight annoyance be produced by it. 

Counterirritation — correction of malocclusion, etc. — may be em- 
ployed. The symptoms may disappear. If they do not, or they 

1 Garretson's Oral Clinic, 1884. 

2 Brubaker. American System of Dentistry. 



654 NON-SEPTIC PERICEMENTITIS 

are severe when the patient applies, the tooth should be completely 
extracted. The operation of amputation of the root end might be 
safely tried for apical hypercementosis, but there are no records of its 
employment as a means of cure. The bulbous condition of the root 
end may cause extraction to be difficult, and fracture of the root end 
may occur. Flagg recommended that in such a case a fissure drill 
be passed about the circumference of the root end to remove the bony 
obstruction to its passage out of the alveolus, after which it may 
be lifted away with tweezers. In another method the root may be 
perforated by a drill and then divided into two sections by means of 
a dentate fissure bur, after which the halves may be pushed together 
with a small elevator. If not then removable the fissure bur can 
now easily enlarge the alveolar constriction. Cocain may be used 
as an obtundent. The use of alveolar forceps for the condition is 
little short of brutal, and only warranted by the impracticability 
of other means. 

Extraction for hypercementosis may cause considerable bruising 
of the walls of the alveolus, followed by excruciating pain lasting 
often for days. The alveolus may refuse to granulate, and a septic 
condition result. The pain has at times been relieved by the injec- 
tion of a 2 per cent, solution of cocain or novocain into the gum 
on either side of the alveolus, after which the surfaces of the alveolar 
walls should be sterilized and burred away until tissue capable of 
granulation is reached. 

The alveolus should then be irrigated and a clot invited by causing 
a slight hemorrhage. (See p. 634.) 

ANKYLOSIS (SYNOSTOSIS). 

By this is meant the union of bone and cementum, a condition 
analogous to ankylosis of bone. 

Hopewell-Smith 1 has described 5 cases, of which he offers the 
following explanation: (1) inflammation occurs and the membrane 
is changed into granulation tissue; (2) the cellular elements destroy 
portions of the bone and excavate the cementum; (3) the mass of 
granulation tissue is then ossified, joining the bone and cementum 
in a firm union. 

E. C. Rice 2 has reported a case of a lady for whom an implantation 
of an upper bicuspid was done. In an effort made later to remove 
the tooth all attempts to loosen it in any degree with forceps failed. 

In my own practice an implanted tooth is firmly immovable in 

1 Histology and Pathohistology of the Teeth. 

2 Private communication. 



RESORPTION OF THE ROOTS OF PERMANENT TEETH 655 

any degree, though several years in place. The union may not be 
a true ankylosis in these cases, though doubtless bone has entered 
areas of previous resorption. A remarkable case was shown the 
editor by Dr. J. Curry, of Philadelphia. Every pier tooth of 
four bridges was firmly ankylosed and immovable, yet large bays 
of resorption in each root necessitated extraction. This was not a 
plantation case. 

Fig. 594 



R 





B- 



Vertical section of a human tooth ankylosed to the jaw: R, root; B, bone of jaw. 
The absolute continuity of the two hard tissues is strikingly shown. From the col- 
lection of the late Storer Bennett. 1 (Hopewell-Smith.) 



RESORPTION OF THE ROOTS OF PERMANENT TEETH. 

By resorption of the roots of permanent teeth is meant the gradual 
removal of the cementum and dentin of permanent roots by phago- 
cytic cells existing in the adjacent soft tissue (osteoclasts). When 
occurring as the result of pressure by another tooth a tissue similar 
to an absorbent organ (See p. 218), as in resorption of deciduous 
teeth, is probably developed between them. 

Causes. — The proximate cause is probably in all cases a degree of 
irritation greater than that required to produce hypercementosis. 
•Probably a mild non-septic inflammation exists. Talbot's demon- 
strations of interstitial gingivitis, a term meant to include interstitial 

1 Transactions of the Odontological Society of Great Britain. 



656 



NON-SEPTIC PERICEMENTITIS 



pericementitis, show that it is a frequent cause of both root and 
alveolar resorption. (See Deeply-seated Gingivitis.) In other 
words, it is due mainly to an aseptic pericementitis. 

The disease has been discussed by other writers as "Rarefying 
Pericementitis," fairly analogous to osteoporosis. (See p. 144.) 



Fig. 595 



Fig. 596 



Fig. 597 






Fig. 595. — Apical abscess and resorption, produced by a protruding broach. 

Fig. 596. — Deciduous cuspid crowned, mistaken for permanent cuspid which lay- 
in jaw and caused resorption of root of permanent lateral. (Skiagraph by Price.) 

Fig. 597. — Resorption at cervical third in two replanted teeth, one broken in 
consequence. Editor's practice. (Skiagraph by Hagopian.) 



Fig. 598 



Fig. 599 





Case of extensive resorption about upper 
central. (Skiagraph by Lodge.) 



Resorption of roots. (Skiagraph 
by Lodge.) 



Of primary causes chronic apical abscess seems to be a frequent 
one. Although theoretically the alkaline pus formed should neutral- 
ize acid formation, the fact of resorption remains, and is probably 
explainable upon the ground that it is produced by the granulation 
tissue formed about the root apex during periods of lessened pus 
formation. 

Protruding root fillings or broaches are common causes (Fig. 595) . 
Plantations are frequently followed by it. A peculiar resorption 



RESORPTION OF THE ROOTS OF PERMANENT TEETH 657 

in the cervical third of two replanted incisors caused the fracture 
of one at the point of resorption and necessitated the removal of 
both teeth (Fig. 597). Plantations are usually followed by peculiar 
resorptions over even the entire root. Looseness of a tooth with the 
resultant excess of movement excites deeply-seated gingivitis and 
resorption of bone and often of roots. Partial luxation as the result 
of a blow or fall produces the same result, the pericementum becom- 
ing thickened, the tooth loosened and extruded, and malocclusion, 
which is also a cause, being induced. 

A toothpick broken off in the gum tissue has produced resorption 
at the neck of the root. 

Fig. 600 




Inflamed pericementum, osteoclasts in Howship's lacunae. (V. A. Latham ) 

The descent of a supernumerary or impacted tooth upon a per- 
manent root has caused resorption, exposing the pulp of the resorbed 
root, and producing pulp reactions. This may be quite extensive 
before violent symptoms occur (Fig. 596). In one case both the 
buccal roots of an upper molar were removed by a supernumerary 
tooth, the crown of which fitted the resorbed root ends. 

Resorptions also occur in orthodontia, as when a cuspid is delayed 

and presses upon a lateral root. The resorption may be more distant 

than the pressure point. In orthodontia this may be explained 

by the extension of the phagocytic area or the induction of such an 

42 



658 NON-SEPTIC PERICEMENTITIS 

area about moving teeth; indeed, teeth cannot be moved without 
exciting a phagocytic action. 

Dewey, 1 following Hertzler, claims that rickets causing imperfect 
calcification of teeth is liable to be a factor in untoward resorptions 
in orthodontia, while tuberculosis neither interferes with tooth, 
eruption nor calcification, but may interfere with proper physio- 
logical resorption because the phagocytes are elsewhere occupied and 
the absorbent organ is not fully developed. 

Calculus beneath the gum margin has produced resorption through 
the production of gingivitis. In one case noted four lower incisors 
presented the characteristic bays at a point one-eighth inch below 
the gum line. 

Some of the cases exhibit no tangible cause; the root resorbs 
apparently as the result of a peculiar reaction upon the part of the 
tissues of the individual, who may lose many teeth by this process — 
i. e., a dyscrasia exists. The teeth may be non-carious and the pulps 
vital. In some of these cases neurasthenia or a uric acid diathesis 
seems to have some association with the condition (Fig. 601). 

Pathology and Morbid Anatomy. — Both resorption of cementum 
and its redeposition occur in deciduous teeth as physiological pro- 
cesses; at some aspect of the cementum the tissue becomes hollowed 
out, and later filled in by new cementum. Resorption of tissue 
throughout the body is accomplished by means of multinucleated 
cells (giant cells, osteoclasts). At some part to be physiologically 
resorbed these cells make their appearance in contact with the 
tissue to be removed, and it gradually disappears, the layer of multi- 
nucleated cells constantly occupying the excavated territory known as 
Howship's lacunae (Figs. 73 and 600). 

If a foreign (aseptic) body be introduced into living tissues, it 
becomes surrounded by these cells, which in some cases effect its 
removal; in others, failing to remove the foreign body, connective 
tissue forms about it and encysts it; encystment may occur after 
partial removal by giant cells. 

The resorption of a root may be of any extent, from a slight spicular 
roughness of the apex of the root to almost complete removal of 
the root. 

Perforation of the root from side to side may occur, of course, 
involving the pulp canal, and, if the pulp be alive, obscure reactions 
upon its part may occur (Fig. 601). 

An area of marked resorption may occur at a point just beneath 
the gum margin and upon any aspect of the tooth. In this situation 

1 Items of Interest, May, 1914, p. 358. 



RESORPTION OF THE ROOTS OF PERMANENT TEETH 659 

it may simulate a cavity of decay beneath the gum. It occurs 
upon either vital or devitalized teeth, and may expose the pulp 
of the root-canal filling. The gum tissue is usually found within 
the cavity. 

It is probable that in plantations the root acts as an aseptic foreign 
body; mild inflammation occurs, subsides, and giant multinucleated 
cells attack the tooth root and endeavor to 
remove it by solution; this they accomplish, FlG - 601 

in part, in spots; then a tolerance is estab- 
lished and connective tissue organizes about 
the roots; later, more complete regeneration is 
represented in the formation of bone; condition 
of a bony fixation is established, evidenced by 
the clear ringing note elicited upon tapping the 
planted tooth. 

T „. . . Idiopathic resorption 

W ltn reference to resorption alter planta- f permanent root. The 
tions, Miller 1 records the following results of ba ^ ;^ on th , e sid f ex ~ 

° . posed the pulp and per- 

1ns observations, the fixation 01 reimplanted forated the root as 
or transplanted teeth mav be accomplished in shown. Crater-like re- 

. sorption about apical 

three Ways: foramen. Pulp first de- 

1. Bv simple encapsulation of the root. vitalized on account of 

n -o ,t i li p • • i-i persistent pam and the 

z. Joy the bundles ol connective tissue which tooth later extracted. 
fill up irregular absorption spaces, especially 

where the pericementum has not been present at that portion when 
the implantation was made (a pseudo-attachment). 

3. By direct union of the surrounding tissues with the living 
pericementum. He inclines to think this the only permanent 
attachment. 

He states that for the most part osteoclasts were few and that 
resorption was carried on by small round cells. 

The inflammatory reaction and resorption is least when replanta- 
tion is practised, but may at times be pronounced in even those 
cases. If the socket of a tooth extracted for resorption be examined, 
a mass of soft tissue will be found occupying the locations corre- 
sponding to the areas of resorption (Fig. 602). No acid reaction can 
be detected with litmus paper, but, nevertheless, it is probable that 
the cells producing resorption excrete an acid capable of dissolving 
the tissue. 

There is some evidence of this in cases of enamel resorption occur- 
ring upon the crow r ns of impacted teeth which have never been in 
relation with the oral fluids, and about which there is no evidence of 

1 Independent Practitioner, 1887 



660 NON-SEPTIC PERICEMENTITIS 

caries in the areas of dentin resorption also present. In the fortunate 
specimens of these cases a superficial decalcification of the enamel 
surface may be seen which can only occur as the result of acid action. 
(See p. 312.) 

Fig. 602 





Diagram of a case of root resorption 
after secondary dentin had formed: SD, 
secondary dentin; AR, area undergoing 
ii resorption; peculiar central spire of sec- 

ondary dentin which has resisted the 
Resorption of distal root of a first resorbent action. Specimen in possession 
molar. (Skiagraph by Custer.) of Dr. A. P. Fellows. 

Symptoms and Diagnosis. — The tooth may present symptoms 
of non-septic pericementitis, and may be loosened in advanced 
cases. In the early stages no looseness may be observed until a 
strain suddenly applied causes a luxation; thereafter the tooth 
progressively loosens. 

The condition may be discovered by accident; evidences of mild 
pericementitis appear, and the pulp canal is opened to search for 
a cause. The pulp may be found alive; if alive, and it is killed, or 
if it is found dead, broaches pass suddenly into the mass of soft 
tissue underlying the root. The progressive loosening of the tooth, 
with its peculiar movement, is about the only constant symptom of 
the condition. 

In cases of live pulp this organ may be hyperemic, so that increased 
response to heat or cold is felt; this, taken in connection with the 
tenderness upon percussion which can usually be elicited, and with 
the peculiar loosening of the tooth, is a diagnostic guide. 

Flagg 1 stated that reflex neuralgias occur in this condition, but 
that the most constant indication noted by him was a sense of dis- 
comfort about the jaws, vaguely associated with some one tooth. 
The patient is convinced that if the tooth were removed relief would 
follow. In the absence of the loosening, which may not occur until 
the root is nearly gone, the resorption is most commonly discovered 
by entering the pulp canal and finding its length much shortened. 
In some cases the resorption may be found near the gum margin and 
simulating a cavity of decay, from which it may readily be diagnos- 

1 Lecture on Dental Therapeutics. 



OVERUSE OF TEETH 661 

ticated by its appearance when exposed by packing the gum away. 
Such cases appear to accompany a marginal gum resorption; 

The .r-rays should exhibit the condition with sufficient clearness 
to furnish an absolute diagnosis. 

Treatment. — If a diagnosis can be made, the tooth should be 
extracted except in the cases near the gum margin alone, which may 
be filled with plastic fillings. Even then the condition may progress. 

DEGENERATION OF THE PERICEMENTUM. 

Strictly speaking, the overuse, abuse, and disuse of the teeth are 
causes which produce a general hyperemia or inflammation of the 
pericementum (non-septic pericementitis). If continued, the inflam- 
mation extends into the gum tissue and a deep-seated gingivitis is 
produced. The results of the causes are, therefore, classifiable under 
either non-septic pericementitis or deeply-seated gingivitis. Either 
of these conditions renders the tissues involved liable to the degen- 
erations and resorptions which accompany continued inflammation, 
or acts as a predisposing cause to local infection by oral organisms, 
beginning its action at the gum margin, and which sooner or later 
produces a purulent, or apparently non-purulent, liquefaction of the 
gingival portion of the pericementum (pyorrhea alveolaris). 

In view of applied therapeutics it is well to consider these causes 
separately. 

OVERUSE OF TEETH. 

By overuse of a tooth is meant such a variety of occlusion that the 
tooth receives a greater stress than its neighbors, or than it is designed 
to bear. The stress may be received in the normal direction, but be 
excessive in amount. The most prominent cause of this condition 
is the loss of one or more other teeth, permitting undue stress to fall 
upon the neighboring teeth, or, in some cases, on far-distant teeth. 
Too prominent artificial crowns, particularly those of the all-gold 
type, cause a general increase of stress upon the pericementum. 
Enormously overful contour fillings may establish a similar condition. 
When but few isolated teeth remain in one denture and have antag- 
onists, the teeth are certain to be overworked. Isolated and other 
teeth to which are attached clasps of artificial dentures or too large 
pieces of bridge-work, are in the majority of cases being constantly 
overstrained. 

Pathology. — Like any other functional part which is overworked, 
the pericementum is first stimulated, causing the vessels to dilate. 
Soon evidences of overwork appear, and the condition passes into 



662 NON-SEPTIC PERICEMENTITIS 

one of interstitial pericementitis; the tooth projects, and is loosened; 
the overlying gum deepens in color, and evidences of venous engorge- 
ment are common (interstitial gingivitis). The result of the con- 
dition is a softening and degeneration of the substance of the peri- 
cementum; the alveolar wall is involved in the degeneration, and it 
melts down — is resorbed to a greater or less extent. Cases have 
been seen at this point with the gum margins as perfect as in any 
normal tooth though a symmetrical resorption of margins may 

Fig. 604 



Illustrating use of overarch bar. See text. Gorman. 1 

be present. In one marked case in which incisors met with a slight 
lingual occlusion upon the lowers, forcing them labially, the teeth 
were as loose as in the average pyorrhea case, but the gum margins 
showed absolutely no pocket. At any stage of the disturbance 
marginal infection may occur, and the degeneration and destruc- 
tion of the pericementum be hastened by suppuration or other 
secondary degenerations establishing pyorrhea alveolaris. 

The symptoms, diagnosis, and clinical history are given in the 
above description. The prognosis is the inevitable loss of the tooth 

1 Items of Interest, October, 1913. 



OVERUSE OF TEETH 



663 



if the causes be not removed, in which event the prognosis is governed 
by the extent to which the degeneration has proceeded. (See 
Interstitial Gingivitis.) These cases are often seen at a time when 
it is difficult to say which came first, the pyorrhea or the overwork, 
but the conditions of evident overstrain, as when posterior occulsion 
is largely lost, and the usually prompt response to surgical rest lead 
to inference that overwork started the predisposition to pyorrhea. 
Nevertheless in pyorrhea when the marginal inflammation has 
caused hone resorption to the point of tooth loosening the mechanical 
strain of occlusion is a cause of further overstrain and looseness. 







Fig. 605 








- 




(i 




| J i i 


i i 






jap 





A case of pyorrhea alveolaris and overwork. Five natural and one artificial tooth 
mutually supported by holding against plate brace. Note restraint of right cuspid 
and central by clasp, artificial tooth bevels and T button and restraint of left teeth 
by clasp and button. This principle may be employed in ordinary plate work. Adap- 
tation made by burnishing thin pure metal to teeth model, and stiffening with solder. 



The teeth, if in overocclusion, should be dressed off until properly 
occluded. Prosthetic appliances should not be so attached by clasps 
as to unduly move the clasp teeth, especially buccolingually. The 
U-clasp is worthy of consideration in this regard. The appliance 
should support the teeth laterally, if possible, and occasionally the 
enclosure of the teeth by the plate clasps, with the hooks facing 
each other or a buccal embracing wire stay, is required, as, for 
example, where four lower bicuspids only are retained for support 
to the plate, yet where they also require support (Fig. 617). Where 
incisors are loose yet teeth must be inserted on plates, the judicious 
shaping of the natural and artificial teeth so as to afford a restraint 



664 NON-SEPTIC PERICEMENTITIS 

of the natural ones against the plate festoon is useful (Fig. 605). 
In some cases the festoon causes gingivitis and tends to cause loosening. 
This may be due to an improper looseness of the clasps permitting 
a rise and fall of the plate, or the inner edge of the festoon requires 
trimming. (A lower bar plate in which no contact except at clasp 
teeth is allowed because the bar lies beneath the tongue level and, 
of course, away from the teeth is an example of the principle involved 
in avoiding this class of injury). No attempt is made, however, 
to cause the artificial teeth to strike before the natural teeth, in 
the hope of giving surgical rest to these organs. Such attempts 
always result in failure, as they cause injuries to the tissues upon 
which the plate and teeth rest, which are more severe than the 
pericemental disturbance. 

Properly adjusted bridge-work frequently does good service in 
these cases, provided the overoccluding tooth or teeth be first dressed 
down short of occlusion and are given a period of rest until the 
pericementum recovers. The bridge, if carefully planned, may be 
made to direct and control the stress received by the injured teeth. 
Joining the various bridges is useful. In this connection what is 
termed the "overarch bar" is a valuable device. The wire crossing 
the palate from one bridge to another on the opposite side automatic- 
ally throws some of the stress received by the diseased teeth upon 
teeth upon the other side of the arch, which naturally are forced in 
an opposite direction during mastication or at least lend their support. 
(Fig. 604 illustrates this.) 

The use of the Gilmore attachment is useful, the wire supporting 
the plate connects several teeth roots and gives them mutual support. 

Improperly occluding artificial crowns should have this fault cor- 
rected by removing the excess of material or by setting properly 
made crowns. All crowns should have full mesial and distal contact, 
as spaces permit a wedging of teeth and injury of the interdental 
gum septum, as well as allow movement to occur. 

Overfull fillings should be reduced to correct proportions and 
shape. 

Surgical rest is the only hope of saving the tooth. 

MALOCCLUSION OF THE TEETH. 

Each tooth of a denture is not only designed to receive a definite 
amount of force, but to receive it in a particular direction or direc- 
tions ; any excess of this force, or alteration of its direction, is followed 
by abnormal stimulation of the pericementum and by its overstrain- 
ing. The effects following a general increase of stress have been 



MALOCCLUSION OF THE TEETH 665 

considered under the previous heading. By malocclusion is here 
meant the constant reception of stress by the pericementum in 
directions to which it is quite unaccustomed, or which are not in 
accordance with the anatomical design of the tooth. It is a peculiar 
form of overuse. 

Causes. — Original malpositions of the teeth may cause their faulty 
occlusion. The most prolific source of the condition is, however, 
altered occlusion due to those changes of position of the teeth which 
follow upon the loss of adjoining teeth. 

Artificial crowns, which do not occlude in correspondence with 
the other teeth are a common cause. Improperly formed fillings 
are another cause. 

The shifting of positions of the teeth, in consequence of patho- 
logical changes occurring in or about the pericementum, causes the 
crowns of teeth to occlude improperly. 

Pathology. — The conditions established are those of overuse in a 
direction other than direct. A typical example of this condition is 
that of a lower second molar which has gradually tilted forward in 
consequence of the loss of the first molar; or a central incisor which 
has altered its position in consequence of secondary formations in 
or about the pericementum, a common precursor of phagedenic 
pericementitis. Some portion of the tooth, an edge, which before 
did not occlude with an antagonizing tooth, is brought into occlu- 
sion; if the occlusion be not unduly forcible, no immediate degenera- 
tive changes are evident. If the occlusion be excessive, the peri- 
cementum is not uniformly affected, but the greatest stress is brought 
to beax upon some lateral aspect of the structure. It responds 
in the degree of the overwork, and inflammation and degenerative 
changes occur, which, if the active causes be not removed, gradually 
spread to other portions of the pericementum, and the phenomena 
noted in connection with overuse occur, but are not so general in 
distribution. The tooth becomes more movable in one or more 
directions — i. e., is loosened; it may develop some degree of tender- 
ness upon percussion, and the gum color toward the affected side 
deepens, although it may remain normal in other parts. As in the 
previous cases, infection may — indeed, is likely to — occur. In 
some cases the pericementum may degenerate and be destroyed 
about one root of a multirooted tooth, and remain about the other. 
It is to be remembered that a less degree of irritation may produce 
hypercementosis . 

Pyorrhea alveolaris in any form is a localized suppurative peri- 
cemental inflammation, which causes inflammation of the peri- 
cementum in general. Swelling occurs and the tooth is pushed up 



666 NON-SEPTIC PERICEMENTITIS 

into malocclusion. Other teeth are sometimes urged out of occlu- 
sion by these. Such teeth may sometimes be dressed off one thirty- 
second of an inch before the overocclusion is relieved. A direct 
result of the strain and compression brought to bear upon apical 
tissue is the production of non-septic pulpitis with reflex pain and 
response to heat and cold (see Fig. 413). 

Diagnosis and Treatment. — In all malposed teeth a careful examina- 
tion should be made of their mode of occlusion. If the tooth exhibit 
tenderness and looseness, malocclusion is almost a certainty; it only 
remains to determine its direction. 

The spots of faulty occlusion may be determined by placing a 
strip of carbon paper (articulating paper) over the tips of the antag- 
onizing teeth and having the patient bite; the spots of contact should 
then be ground away until the tooth is slightly short of direct occlu- 
sion. Fresh strips of paper are used, and the jaws moved laterally, 
as in mastication, to note other points of contact; these should also 
be ground away. 

It suffices in some acute cases to place a rubber dam or metal cap 
guard upon a nearby tooth for a day or two to prevent occlusion 
upon the sore tooth, which regains its normal position in the alveolus 
as the inflammation subsides. The grinding and guarding may be 
combined, judgment being required. 

Prognosis. — If the condition be not corrected every time occasion 
requires, the degeneration progresses until the tooth is lost. 

If marginal infection has occurred, purulent or non-purulent 
marginal pericemental liquefaction (pyorrhea alveolaris) may have 
to be considered. 

DISUSE OF TEETH. 

Definition. — By disuse of teeth is meant a degree of usage less than 
the amount which the forms and structure of the teeth and contiguous 
parts fit them for. The disuse may be absolute or relative; teeth 
may not occlude at all, owing to the loss of antagonists or to extremely 
irregular positions. 

Partial Disuse. — Causes and Pathology. — If soft food be used 
instead of that requiring vigorous mastication, or if one tooth of a 
side be diseased so that that side of the mouth is unused in mastica- 
tion, or if one of the antagonists of a tooth be lost, the pericementi 
of the teeth involved do not receive their proper amount of exercise, 
and a degree of atony ensues. 

This partial disuse has a more distinct relation to the health of the 
gum margin, which does not receive a normal amount of friction 



DISUSE OF TEETH 667 

from mastication, and if this be not offset, in part, by prophylaxis, 
marginal gingivitis ensues. 

Infection and the formation of calculus increase the irritation to a 
marginal gum inflammation, which is liable to run into a pyorrhea 
alveolaris. This is the real significance of disuse as a cause. 

Diagnosis and Prognosis. — A diagnosis of disuse (relative) is usually 
made out by inquiring as to the food habit of individuals. It is 
excessively common in civilized communities, particularly among 
the well-to-do, and is of almost constant occurrence in gourmands. 

Treatment. — Patients should have pointed out to them the results 
of insufficient mastication, together with the evils of faulty oral 
hygiene. Every effort should be made, by the use of constant 
prophylactic measures, to forestall the occurrence of pyorrhea 
alveolaris. This and similar conditions are particularly to be feared 
in the degenerative periods of early and late middle age. It is 
between the ages of thirty and fifty years that ill-consequences 
are most to be feared from acquired debility of the pericementum. 

Absolute Disuse. — Teeth which perform no work directly in masti- 
cation, or indirectly by serving as abutments for a bridge-piece, 
may be said to be in a condition of absolute disuse. 

Results. — A tooth or root whose pericementum receives no stimulus 
becomes relatively a foreign body to the organism. It is a useless 
part, and the body attempts to cast it out. Perhaps these phrases 
are insufficiently exact; however, a disused tooth is lost through a 
series of pathological changes. It is probable that the impact of 
blood pressure raises the tooth an infinitesimal distance, and being 
without antagonism it does not wholly recover its normal position. 
The aggregate of these infinitesimal differentials being expressed in 
protrusions, probably lack of accustomed pressure allows a slight 
overfulness of blood with further increased blood pressure (see p. 
123). Devitalization of the pulp sometimes lessens this. 

This is a fairly rapid process, and occurs often after the trim- 
ming of teeth for bridge-work so as to interfere with the planned 
occlusion, unless the bridge be rapidly made. If unopposed, it 
extends progressively, the neck being usually exposed, though some- 
times the alveolar process becomes developed and lies on a lower 
level as though it had followed the tooth down. Usually the bifur- 
cation of a molar becomes exposed, calculi form, and the extrusion 
becomes hastened by marginal gingivitis. The tooth may be firm 
.even though half its root length be exposed, though often it becomes 
looser than normal. Sometimes it strikes other teeth with a glancing 
motion. If the teeth in Fig. 606 were closer this would occur, and 
such a process (malocclusion) hastens the loosening. The opposite 



NON-SEPTIC PERICEMENTITIS 

gum may be injured by such a tooth. Another effect is the wedging 
of food between the teeth owing to a favoring entrance, the laterally 
unsupported tooth wedging apart and then closing upon the food. 
This injures the gum septum. (See Gingivitis.) 

Finally the loosening or the annoyance compels the removal of 
the tooth. 

The danger of marginal infection is always great in these cases. 
Some degree of infection, no doubt, exists in all of them, which 
serves to explain the increased rapidity of the degenerations. 

Fig. 606 



Absolute disuse and elongation of an upper and a lower molar; partial disuse of 
bicuspid; small abscess cavity in the bone about a root. (Philadelphia Dental 
College Museum.) 

Prognosis. — If teeth can be directly or indirectly brought into use, 
so that their pericementi receive exercise, the cases may recover, 
provided the atrophic changes are not very pronounced; in which 
event the atrophy proceeds, although more slowly. Teeth crowned 
or made abutments for bridges, after degenerative changes have 
become established — i. e., when the normal pericementum has been 
replaced by a thickened mass of partially organized connective tissue 
— usually become progressively looser; the alveolar atrophy proceeds 
until all attachment is lost. 

If this principle be utilized early, the teeth may be saved. The 
results are better if the teeth or roots be utilized before the age of 
thirty than at later ages. 

Treatment. — The treatment consists in bringing the teeth into use, 
if the degeneration has not proceeded too far. In crowning for a 
bridge pier it is customary to shorten the crown to the general occlusal 



FIBROID DEGENERATION OF THE PERICEMENTUM 669 

level, though even if a little longer and not in direct occlusion the 
tooth is brought into a sort of mastication which is useful if it does 
not introduce an element of malocclusion, i. e., if the distal or repelling 
strain upon its mesial slope is compensated for by the mesial strain 
upon a pier or piers more mesial to it, or upon a pontic tooth, for 
example, upon the cuspid of Fig. 606, or pontic bicuspid occluding 
with the mesial slope of the lower first molar. In such a case as this 
grinding both the upper and lower molar occlusally and the intro- 
duction of an upper bridge is indicated. Later, extraction is inevit- 
able. The operation, when determined upon, should not be delayed, 
for not only are bacterial growths invited about the loosened tooth, 
but the soft tissues are frequently increased in volume, and if extrac- 
tion be delayed until complete local atrophy of the alveolar walls 
has taken place, a soft and spongy mass remains, which interferes 
with the comfortable wearing of prosthetic appliances in the future. 

FIBROID DEGENERATION OF THE PERICEMENTUM. 

Fibroid degeneration of the pericementum is a senile atrophic 
change occurring in teeth, the pericementi of which have run a 
healthy life course, but finally have become subject to senile marantic 
constitutional changes of not clear nature. The condition thus first 
defined by Hopewell-Smith 1 is further described as found in that 
class of teeth of the aged which have resorbed alveolar margins and 
exposed cementum, but not necessarily subject to pyorrhea areo- 
laris, though traumatic pericementitis may be present. In some 
cases the teeth may be firm. 

Pathohistology. — The chief characteristics are an increase in size 
of the fibers of the pericementum, the loss of their nuclei, their 
generally structureless character, and their arrangement in promi- 
nent bundles about large spaces (areolae). (See Fig : 607.) 

The fibers are firmly implanted in both bone and cementum. The 
cementum does not become hyperplastic (hypercementosed), but 
the bone becomes osteoporous and the Haversian canals contain a 
shrunken fibroid tissue resembling that in the pericementum (Fig. 
608). 

The gum tissue in the vicinity also undergoes retrogressive changes 
in sympathy, becomes less vascular and more fibroid. 

The condition may persist without inflammatory or suppurative 
changes, though it may act as a cause of obscure neuralgia or as a 
predisposing cause to pyorrhea alveolaris. 

1 Dental Cosmos, 1904. 



Pig. 007 




----- C 



Fibroid degeneration of the pericementum: C, cementum; A, alveolus; F, fibers 
with decrepit nuclei. Transverse section. (Hopewell-Smith.) 

Fig. 608 




H 



A _ 



V 




M 



Fibroid degeneration of the pericementum: C, cementum; M, degenerated peri- 
cementum; A, alveolus; H, enlarged (osteoporous) Haversian canals. Transverse 
section. (Hopewell-Smith.) 



ACCIDENTS TO TEETH ■ 671 

Hopewell-Smith points out that the areolar spaces may admit 
microorganisms to deep parts, thus predisposing to antral disease or, 
possibly , osteomyelitis. 

ACCIDENTS TO TEETH. 

Apart from fracture of the teeth by accident, several interesting 
accidental conditions involving therapeutics require consideration. 

Teeth Driven into Alveolar Process. — Blows, falls, etc., have occasion- 
ally caused teeth to be driven forcibly into the jaw- . The condition 
may be complicated by fracture, in which case the judgment of 
the operator must be exercised. If the tooth be not fractured 
it may be drawn dowm with forceps and ligated in place until firm. 
The use of zinc phosphate upon the ligatures, if possible to use it, 
renders them more rigid. Splints may be used. If evidence of pulp 
death be noted by subsequent test, or apical pericemental inflam- 
mation, the pulp should be removed. 

Luxation or Partial Dislocation by Accident. — Teeth may be par- 
tially knocked out and driven either lingually or buccally. The pulp 
connections will be ruptured, as a rule, but after asepsis of the parts 
by means of antiseptic sprays the teeth may be pressed into place, 
and if ligated or splinted may again become firm by deposition of 
bone about them. The pulps nearly always give evidence of death 
so that they should be later replaced by canal fillings. 

Mendel Joseph and Dassonville 1 record experiments on dogs 
showing a vital attachment of the pulp of an immediately replanted 
tooth. .They used strictly aseptic precautions. 

Occasionally evidences of reattachment of pulp have been recorded 2 
even after total displacement. If the accident result in elongation 
of the tooth with production of a chronically spongy pericementum, 
the operation of replantation should be performed. 

Total Dislocation of Teeth by Accident. — If the accident result 
in total displacement from the mouth, the tooth or teeth may be 
prepared as for replantation (see p. 624), and under aseptic pre- 
cautions replanted in their alveoli. If held by ligatures or splints 
they will usually become firm. If the teeth are kept moist a short 
delay if necessary does not prevent success, though clot and granula- 
tions must be swept out. 

Attachment of Teeth. — Tw t o or more teeth may be attached by the 
intervening alveolar process, fracture of w r hich may cause both teeth 
to be removed in extraction. In a few cases of loose deciduous teeth 

1 L'Odontologie. See Dental Cosmos, 1906, p. 1060. 

2 Kirk and W. Trueman. 



G72 NON-SEPTIC PERICEMENTITIS 

the gum has been sufficient attachment to cause the removal of two 
teeth at once. 

In some cases the tough, fibrous nature of the pericementum 
causes the alveolar bone fractured by the leverage upon it to remain 
attached to the tooth, and Fig. 210 illustrates teeth attached by 
union of pericementum only. 

Fracture of the Alveolar Process. — Slight fractures of the alveolar 
plate are of little consequence, as a rule. In some cases one plate 
may be fractured, and unless removed with the tooth, may usually 
be pressed back into place. Reunion may be looked for if asepsis 
be maintained. Fractures of the alveolar process from blows, 
kicks, etc., upon the jaw may become septic and sequestra may 
form, necessitating removal of both bone and teeth. Such fractures 
should have immediate attention. Fractures of the maxillse should, 
of course, be immediately reduced. 

Hemorrhage following Extraction. — Even in the absence of hem- 
ophilia postextraction hemorrhage may be somewhat severe, and 
is well controlled by a little tannic acid or powdered alum and thymol 
upon a pellet of cotton, or nosophen gauze wet with phenolsodique. 

If necessary a linen compress should be placed over it and a Barton 
or Garretson bandage applied. The internal use of calcium chlorid 
or other hemostatic is indicated if the bleeding be continued. (See 
p. 120.) 

Lacerations. — The tongue, floor of the mouth, etc., may be lacer- 
ated by the careless use of forceps, and the lacerated parts should 
be irrigated with antiseptics and the mouth kept under astringent 
antiseptics while the parts are healing. Lacerated gum margins 
should be trimmed up to prevent sloughing. 

Postextraction Alveolitis. — This has been already discussed. (See 
p. 633.) 

For ordinary transient pain, phenolcamphor with or without 
menthol added or equal parts of phenolsodique and laudanum are 
useful. Hot salt water held in the mouth is analgesic, styptic and 
stimulant. 



SECTION VI. 

PERICEMENTAL DISEASES BEGINNING AT 
THE GUM MARGIN. 



CHAPTER XXII. 
GINGIVITIS. 

The diseases which begin at the gum margin are all inflammatory, 
and are due to mechanical, chemical, and infective local irritants, 
and probably may be due to overexcitation of the gum tissues by 
leukomains or other toxic products which are formed intrinsically 
within the body in malnutritional processes, also to overexcitation 
by certain drugs, both of which the gum is endeavoring to eliminate. 
The inflammation resulting is termed gingivitis. Many mechanical 
or septic causes which produce pericementitis, such as overuse or 
apical abscess, finally induce an inflammation in the alveolar bone 
(osteitis), and later an inflammation of the gingival tissue. In 
reverse order, inflammations beginning in the gum, reach the bone, 
and later the pericementum. It is plain then that pericementitis and 
gingivitis are often associated, and at the gum margin are almost 
inseparable. 

If at any stage of a gingivitis, whether of mechanical or chemical 
primary causation, infection enter the inflammation becomes septic, 
and if pyogenic bacteria are the infective agents, pus is formed. At 
this juncture there is a pus flow from beneath the gum margin, 
usually from a pocket extending into the substance of the perice- 
mentum or the location previously occupied by it in the alveolus, 
and from this fact it is called pyorrhea alveolaris, though a variety 
of pyorrhea is apparently non-purulent. Some writers treat of all 
cases of gingivitis as cases of pyorrhea, advanced or incipient, and 
in view of the fact that a simple gingivitis may become a pyorrhea 
there is some justification from a preventive standpoint; nevertheless, 
there are so many phases of gingivitis that for purposes of discussion 
and applied therapeutics it is advisable to specify the various forms 
that may exist. 

43 ' (673) 



674 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 

If confined to the gum margin it is properly designated marginal 
gingivitis; if the inflammatory elements (leukocytes and exudates) 
have infiltrated the deeper connective tissues it may be called deeply 
seated gingivitis or interstitial gingivitis. If a pus flow from the 
alveolus accompany the deeply seated gingivitis the condition of 
pyorrhea alveolaris is established. 

With any of these conditions an hypertrophy or an atrophy may 
be associated, which, on the one hand, may result in hypercementosis 
or exostosis or thickening of gum, or, on the other, in resorption of 
gum or bone. 

MARGINAL GINGIVITIS. 

Definition. — By marginal gingivitis is meant an inflammation con- 
fined to the margins of the gums about the necks of the teeth. 

Causes. — The causes of marginal gingivitis are local and general, 
which may be subdivided into predisposing and exciting. Both 
local and general causes may be in action at the same time. 

Local Causes. — Marginal gingivitis may be excited by the pres- 
ence of food masses or unremoved collections about the necks of 
teeth, their fermentation liberating chemical products more or less 
irritating. Miller 1 has shown that the materies alba about the necks 
of teeth may have either an alkaline or acid reaction, and the gums 
be inflamed. 

The lack of contact or too light contact of approximal surfaces, 
whether due to faulty operations or induced by the wedging action 
of tooth-picks or floss silk, causing a general non-septic pericementitis 
and bone resorption (looseness of teeth) are contributory to the 
wedging of food. 

Bacterial plaques not unlike those producing dental caries have 
been shown by Miller 2 to be formed upon many surfaces of the teeth 
even when no ill results are notable. In practice staining the teeth 
with tincture of iodin will readily demonstrate the presence of such 
bacterial films. Under favoring circumstances these no doubt 
produce marginal gum irritation, a fact proved by the relief of such 
a condition by prophylaxis — i. e., the removal of the plaques. 

Talbot 3 has demonstrated that a deep pocket may normally exist 
at the gum margin favoring the retention of food and other debris. 

Mechanical causes produce direct irritation; these are deposits of 
salivary calculus resting upon the gum or beneath the gum margin; 
fillings projecting beyond cavity margin; edges of poorly fitted crown 
band and the putrefaction of food, etc., collected in the places from 

1 Dental Cosmos, 1894. 2 Ibid, 1902. 

3 Intestitial Gingivitis. 



MARGINAL GINGIVITIS 675 

which cement has washed out; gum overlying cavity margins; bruising 
of the gum margin by food crowded between teeth and removed 
by toothpicks; the fermentation of such crowded food (see p. 683); 
the mechanical action of toothpicks or floss silk improperly crowded 
upon the gum margin; projecting edges of artificial crowns or bits 
of cement used in their cementation; toothbrush bristles; fragments 
of toothpicks, bones, or oyster-shells, etc.; rings of rubber or of torn 
rubber dam or ligatures left in position; rubber or tape wedges 
forced into the gum; the crowding back of a gum by ligation 
which produces ischemia for hours; improper contact of the edges 
of prosthetic plates or appliances about the necks of teeth; injuries 
inflicted by rubber dam clamps, wedges, ligatures, etc.; the eruption 
of teeth through the gums. 

An interesting case of recurrent epileptic attacks was proved due 
to a toothbrush bristle forced into the gum. 1 

The action of any of these causes may be complicated through 
the infection of the mechanically irritated part by oral bacteria. 
An excellent example occurred in the editor's practice. A perfect 
gum margin was irritated by the margins of a gutta-percha cap 
used as a remedy for hyperemia of the pulp. Pyogenic organisms 
produced a marginal suppuration which subsided upon removal of 
the cap. 

All forms of marginal gingivitis are to be considered as incipient 
inflammations which, let alone, may lead to deep-seated inflammation 
and tissue destructions collectively called pyorrhea alveolaris. 

Excessive smoking and the use of alcoholic liquors produce local 
irritative effects, resulting in catarrhal stomatitis and gingivitis. 

Lack of exercise or brushing of the gums produces an atonic 
condition of the gum margin, predisposing to gingivitis of infective 
character. Too persistent brushing with stiff brushes may be 
equally injurious by causing marginal irritation. 

A variety of ulcerative marginal gingivitis exists which tends to 
rapidly penetrate the pericemental tissue and may cause pyorrhea. 
The gum margin has a pasty, sloughing appearance, and the gum 
about several teeth may be involved. Vaughn 2 describes it as 
covered by a grayish necrotic covering which when rubbed off leaves 
a sensitive bleeding surface, the deposit being accumulated rapidly 
in an hour or two. He found the bacillus fusiformis and spirillum 
which work in symbiosis in Vincent's angina. In the severe cases 
he describes fever, dysphegia, headache, malaise, nausea, marked 
salivation, loss of appetite, increased cardiac and respiratory action, 

1 Dental Cosmos, 1910, p. 594. 2 Ibid., 1912, p. 651. 



076 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 

and glandular enlargement as associate phenomena. The breath is 
offensive and characteristic. Syphilitic chancre may begin at the 
gum margin, and there is no reason why aphtha? should not be so 
located though usually elsewhere. 

A form of phagedenic pericementitis causing very rapid destruc- 
tion of the pericementum and loss of the teeth without loss of alveolar 
wall has occasionally been noted. In one notable case two upper 
incisors came away three weeks after an ulceration appeared about 
their gum margins. The patient wore the teeth for several weeks 
in situ, -and could remove and reinsert them at will. The alveolar 
walls were bare, but intact. There was but little pain. The sockets 
healed after removal of the teeth and the freshening of the bone. 
The clinical features of this case were entirely distinct from those 
of the phagedenic condition recognized as phagedenic pericementitis, 
and w T ere more probably caused by the Vincent bacteria (Fig. 611). 

Cook has shown that stimulant and astringent washes, if used 
to excess, have a degenerative influence upon the gum margin. (See 
p. 84.) A too powerful formaldehyd wash has the same effect. 

The production of deeply seated gingivitis by causes of systemic 
or drug origin involves a marginal gingivitis, but marginal gingivitis 
is not always produced by local causes of interstitial gingivitis; at 
least, not at first (see p. 648). 

Systemic Causes. — These are the same as for Deeply Seated Gingi- 
vitis, which see. 

Pathology. — The pathology of marginal gingivitis is that of an 
inflammation located in a peculiar situation — i. e., in the marginal 
gum tissue — and tending to spread into the deeper interstitial tissues. 
(See Pathology of Deeply Seated Gingivitis.) As shown above 
when pyogenic bacteria enter, a pus flow or pyorrhea is established. 

Symptoms. — The symptoms of marginal gingivitis depend upon the 
cause and degree of inflammatory action. When mechanical 
causes are acting the gum presents an inflamed appearance; it is 
swollen, of a bright red or purplish color, very sensitive to touch, 
and bleeds readily. 

If a calculus rest against the gum, the latter may present a raw, 
chronically inflamed surface in contact with it. A ragged, red, 
split margin of gum is often associated with calculus upon the labial 
surfaces of lower incisors, cuspids, and bicuspids, and upper cuspids 
and bicuspids. At times the lingual surfaces of the lower incisors 
present such an appearance. If subgingival calculus be present, 
the gum margin, if markedly affected, appears loosened, and is of 
a flabby appearance and purplish in color. In some cases the gum 
margin appears thickened or hypertrophied. 



MARGINAL GINGIVITIS 677 

A bloodshot appearance — i. e., enlargement of terminal vessels — 
is often seen in gingivitis. 

In cases due to unhygienic conditions — i. e., food collections or 
vitiated secretions about the necks of teeth — a raw, red, outer 
surface of the gum margin is noted, particularly in young persons. 

In stomatitis ulcerosa a yellow, pasty ulceration of the gum mar- 
gins may occur. It is rodent in character, very painful, and may 
cause rapid loss of the pericementum and of the tooth. (See Vincent's 
Angina and p. 681.) In gingivitis due to oral infection by the coccus 
of gonorrhea an intense gingival inflammation with looseness of 
the teeth, pyorrhea alveolaris, and profuse salivation, may occur. 1 

Talbot 2 describes a greenish-gray glazed surface of ulcerated 
raw gum in two cases of profuse interstitial gingivitis due to the 
gonococcus. 

Stein is inclined to doubt the etiology. 3 

The calssification of the gingivitis depends upon the cause and 
progress of the disease. 

Prognosis. — If the case has run an acute course and is due to the 
action of mechanical causes plus infection, recovery is usually prompt 
upon the removal of the cause and sterilization of the injured part. 
In the chronic cases due to the more slowly acting mechanical and 
infective causes combined — e. g., salivary calculus plus infection 
— much deeply seated gingivitis may have occurred accompanied 
by pericemental and alveolar resorption. This usually constitutes 
a permanent loss. If the gum margin is in a state of atony or inflam- 
mation as the result of collections of bacteria, etc., upon the cervices 
of the -teeth, their condition may be improved by frequent prophy- 
laxis. 

Treatment. — The treatment of the condition consists in removing 
the source of irritation and restoring the normal circulation in the 
parts. If the source of the disorder be in some underlying constitu- 
tional condition, the symptoms may be ameliorated, although not 
entirely cured, by the correction of the general disorder. 

Cases due to mechanical irritation are commonly confined to one 
or several teeth, rarely to an entire denture, except cases continued 
in consequence of deposits of scaly calculi beneath the gum margin 
or under plates. Foreign bodies, such as bristles and fragments of 
bone, should be removed. Projecting fillings or overhanging crown 
margins should be made flush with the general tooth surface. Sali- 

1 Vines. British Journal of Dental Sciences, 1903, and Dental Cosmos, 1903. 

2 Dental Cosmos, 1905. 

3 Bacteriology in its Relationship to the Oral and Nasal Cavities. Items of Interest, 
1914. 



678 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 

vary calculi should be removed. When food crowds upon gum 
margins between teeth, lateral or mesiodistal contacts should be 
established either by contouring filling, introducing a bridge which 
establishes such proximal contact, or in some cases by wedging at 
some convenient point so as to crowd several teeth together, then 
introducing a contour filling or inlay. The contact should exist 
just a little to the gingival of the marginal ridges and not be too broad 
and should be well rounded. 

In another phase of this condition in the writer's own mouth the 
extraction of a lower third molar allowed the distal cusp of the 
lower second molar to wedge between the upper second and third 
molars, so that the third molar was pushed distally and shredded 
food packed in simultaneously causing extreme and annoying gingi- 
vitis. In such a case if grinding the cusps of the antagonizing 
molars does not relieve, only extraction or firm attachment of the 
third and second molar will give relief (Fig. 609). In a few similar 
cases where fillings were present the fillings have been overcontoured 
and an iridio-platinum wire imbedded in a groove in one filling 
and the other pointed end allowed to rest in a slight groove in the 
adjoining filling. In this it plays freely but prevents the crowding 
of food, though food may float in laterally without direct injury. 







Fig. 609 










fe*--^^^^8 


^T- J0P 








m*wSm- 








J^L 






M 



Marginal gingivitis located in septal tissue between upper second and third molar 
(see text). Also shows anterior drifting of second molar, due to extraction of first 
molar early in life. 



' This condition frequently results when a bridge has been inserted 
from a second molar forward. The third molar moves away. If 
any looseness of teeth exist it may be better to include the third 
molar as an abutment. 

A further possibility lies in the use of a crown on the third molar 
with a hook or mortised piece attached, which hook or mortise plays 
in a suitable pocket in the crown attached to the bridge, or the pin 



MARGINAL GINGIVITIS 



679 



referred to may play in a groove. Some cases of bridge work are 
constructed with hook attachment, said hook playing in a specially 
made inlay in a tooth not otherwise included in the bridge (Fig. 
610). 

Fig. 610 




Pin embedded in filling in third molar and extending into a groove in filling in 
second molar. Extension plays back and forth but protects gum. 

Any associate pyorrhea due to this cause is usually rapidly cured 
by this establishment of contact. 

Following this, perfect cleansing of all teeth is indicated, this to 
be maintained by monthly prophylaxis, at least until the case is 
cured and then continued periodically for prevention. 

Antiseptic mouth washes should be employed frequently, no 
matter what the cause. If the gum tissue be soft and spongy, 
showing signs of venous hyperemia, antiseptic astringent mouth 
washes should be freely used: 

~fy — Zinc, chlorid gr. x 

Aquae menth. pip fgj — M. 

Increase as desired. 

The above preparation, used in spray from an atomizer, or, if 
diluted, as a wash several times a day, is an excellent local application, 
meeting both indications. Prescriptions containing eucalyptus and 
benzoic acid are excellent: 

3- 



-Acid, benzoic 


3 parts 


Tinct. eucalyptus 


15 parts 


01. menth. pip 


1 part 


Alcohol 


100 parts 


Saccharin 


2 parts — M. 




(Miller.) 



The above formula diluted one-half is agreeable and efficient. 
An alkaline 1 per cent, salicylic acid wash is useful, not only for 
the gingivitis, but any attendant fetor of breath : 

1$ — Sodii boratis 3iss 

Acidi salicylici gr. xv 

AquaB menthae pip f§iij — M. 



680 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 
The following is astringent and antiseptic: 

1$ — Borogb'cerini, 

Tinct. kramerise, 
Tinct. calendulae, 

Alcoholis aa f S J — M. 

Sig. — One or two teaspoonfuls to a small glass of water. 

Truman advises the use of hydronaphthol in an astringent vehicle 
as an effective germicide for use by a patient: 

1$ — Hydronaphthol gr. x 

Glycerol fgj 

Alcohol fgj 

Aqua? destil fgj — M. 

Sig. — Use as a wash several times a day. (PierceJ 

Talbot recommends for gingivitis the following : 

1} — Zinc iodid 15 grams 

Iodin 25 grams 

Glycerin 50 grams 

Water 10 grams — M. 

Sig. — Apply to gum on cotton wound on an applicator and dry after each 
painting. (Talbot. 1 ) 

The following is a 5 per cent, formaldehyd solution which, diluted, 
can be used as a mouth wash, having astringent and antiseptic 
qualities. It is also useful in various strengths as a germicide for 
root canals. A formula for quantity is given, which may be reduced 

in prescriptions: 

No. l 

I}— Thymol 3iss 

Menthol 5ss 

Oil of ecucalyptus, 
Oil of gaultheria, 
Oil of cassia, 

Oil of cloves . aa f 5iss 

Alcohol fgij— M. 

No. 2 

Formaldehyd, 40 per cent, sol Oj 

Boric acid, 

Sodium biborate aa 5hj 

Water Oij— M. 

No. 3 
Water to gal. j 

Make up Xo. 1 first and shake well. Place Xo. 2 in a gallon 
demijohn and shake well; add Xo. 1 and shake again; add Xo. 3 
and shake well. For dispensing this may be filtered; for ordinary 
use this is not necessary. For mouth use one-half teaspoonful is 
to be diluted in two ounces of water, making a 1 to 600 formaldehyd 
solution. 

1 Dental Cosmos, 1905, p. 1312. 




MARGINAL GINGIVITIS 081 

Equal parts of Listerine and ordinary distillate of hamamelis is a 
useful combination. Glycothymolin is a very popular proprietary 
month wash. Lavoris and Vermis lotions are agreeable zinc chloride 

washes when used as directed. Phenol-sodique, 1 to 7 of water 
is quite useful. 

For mercurial gingivitis and stomatitis the following has been 
rationally recommended : l 

1$ — Tinct. myrrhae f3iij 

Potassii chloratis 3ss 

Sodii chloridi 3ij 

Aquse dis q. s. ad fgviij — M. 

Sig. — Use as mouth wash. Repeat every two hours. 

Fig. 611 

%■ ' :. m 

* *:■; • 

^>" 

[ _^LL- — ^"^ 

Showing Vincent's bacteria. (Lederer.) 

All mouth washes require an application of about two minutes' 
duration at least twice a day after cleansing the teeth in order to 
produce the best effects. As this is somewhat fatiguing to the oral 
muscles, several applications may be made, one after the other, 
until the total is attained (Fig. 611). 

In the ulceration gingivitis due to Vincent's bacteria the editor 
has found the following useful as a germicidal wash: 

1$ — Hydrargyri bichloridi gr. j 

Aquae hydrogenii dioxidi f 3iv — M. 

Sig. — Use several times a day. 

] Medical Press, via Dental Cosmos. 



682 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 

Vaughn 1 recommends silver nitrate 15 to 30 grains, water fgj, 
Lugol's solution, chromic acid 10 per cent., zinc chlorid 2 per cent., 
and argyrol full strength. Lederer uses salvarsan (see p. 787). Curette- 
ment is sometimes necessary. Kirk 2 recommends in addition local 
application of tincture of iodin and irrigations of hot water. The 
glandular enlargements require a cold compress or the ice bag. 

For the restoration of gum tissue between molars and bicuspids 
L. Ashley Faught 3 has recommended applications of 10 per cent, 
trichloracetic acid on an orange-wood stick every day or two until 
the case is cured. 



DEEPLY SEATED GINGIVITIS 4 (INTERSTITIAL GINGIVITIS, 

TALBOT). 

Definition. — This may be defined as an inflammation characterized 
by the presence in the deep connective-tissue elements of the peri- 
cementum and gum tissue of an excessive number of leukocytes, 
attracted thither by a general or local irritation of the tissue men- 
tioned. 

Local Causes. — Any of the local causes producing marginal gin- 
givitis, if acting deeply, may produce a deeply seated gingivitis. In 
addition to these, the eruption of teeth, the wedging of them, or 
their movement in orthodontia, the overuse, malocclusion, or dis- 
use, in short, any of the causes of pericementitis, septic or non- 
septic, if producing inflammation extending beyond the confines of 
the pericementum, are causes of deeply seated gingivitis. Pyorrhea 
alveolaris is a suppurative deeply seated gingivitis and pericemen- 
titis combined. Ulceration and necrosis following extraction cause 
gingivitis (see p. 633). 

If at any time pyogenic infection occur at the gum margin, the 
purulent phenomenon of pyorrhea alveolaris is produced. It is to 
be understood that deeply seated gingivitis presents many of the 
features of pyorrhea alveolaris and that the latter is a gingivitis. 
The conditions are, however, pathologically separable. 

The following is a good example: A lady presented an upper 
first molar which had had a pyorrhea which had been cured by 
treatment of gum margins and the mesiobuccal root amputated. 
There was no longer any appreciable pus pocket, but the tooth 

1 Dental Cosmos, 1912, p. 655. 

2 American Text Book of Op. Dent., p. 300. 3 Dental Cosmos, 1905. 

4 The writer has introduced the term to replace interstitial gingivitis, not to multiply 
terms, but because it indicates fairly the anatomical situation. Strictly speaking, 
all inflammations are interstitial. 



DEEPLY SEATED GINGIVITIS 683 

overoccluded one-sixteenth inch and had tipped forward. It was 
not supported mesially or distally by adjoining teeth. It was loos- 
ened. The overocclusion was removed by grinding, the tooth was 
wedged against its mesial neighbor, and a distal amalgam filling 
contoured out to its distal neighbor, thus affording support in the 
direction of its movement in mastication. It became much firmer. 
The writer considers this case as presented for diagnosis one of 
deeply seated gingivitis due to malocclusion and non-support, and 
not a case of pyorrhea. In like manner each case should be con- 
sidered on its own symptoms. 

When food enters the interproximal space it crushes the gum 
septum and later depresses it. The inflammation causes its absorp- 
tion as well as that of the bone septum, so as to leave the buccal and 
lingual portion higher. This may also be inflamed and further 
depressed. The pericementi of both teeth suffer necrosis to the 
gum level. The pocket generally finally suppurates and a lateral 
abscess may result from this cause. 

While this may be classified with pyorrhea alveolaris it seems to 
the writer rather a distinct form of deeply seated gingivitis, at least 
until the pus flow is established. The writer has seen another form 
of this condition in which caries at the linguocervical aspect of two 
molars permitted food to pack laterally (not from the occlusal) 
under tongue pressure. The decay proceeded up the sides of the 
lingual and buccal root adjoining, and a large pocket formed, the 
gum being stripped away. The wedging out of the gum, touching 
with silver nitrate after cavity preparation, filling with amalgam, 
and polishing reduced the pocket to a simple one. The gum grew T 
in as far as it could, and the part remains relatively healthy, without 
pyorrhetic symptoms, but food collects and the condition may become 
worse again. In another part of the same mouth pus was found 
exuding from beneath the ulcerated flap of gum overlying a lower 
third molar. Otherwise the patient's teeth exhibited no pyorrhea. 
Such cases might be considered pyorrhetic if pyorrhea is to include 
all pus flows from the alveolus, but then we must consider apical 
abscess such. The writer believes it better to differentiate the 
conditions. 

Systemic Causes. — Systemic causes act to produce a deeply seated 
gingivitis. Drug or metal poisoning, or auto-intoxication, whether 
gastro-intestinal or by leukomains, and acute infectious diseases, 
a,re systemic causes. 

A case of spontaneous loss of all but one of the upper teeth, with 
subsequent complete alveolar atrophy as the result of the trophic 
disturbance from peripheral neuritis in a tabetic woman, has been 



684 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 

reported by Gaucher and Dobrovici, the diagnosis being confirmed 
by trophic disturbance in the foot followed by plantar perforation. 

It seems quite certain that in conditions of general faulty metab- 
olism substances are generated in the system or are retained by 
reason of faulty elimination, and which, floating about in the blood 
stream, act as irritants to the pericementi and gum margins about 
the teeth. 

Moreover, the pericemental glands seem to be eliminating organs 
which may become overstimulated and thus diseased. 

In all general nutritional disorders parts peripheral to the circu- 
lation are most affected, become debilitated, and tend to a degener- 
ative metamorphosis of cells. 

Rhein found, after repeated examinations of hospital patients, that 
"marginal gingivitis was an accompaniment of typhoid fever, tuber- 
culosis, malarial disorders, acute rheumatism, pleurisy, pericarditis, 
and syphilis, among the acute diseases. Of chronic nutritional dis- 
eases, it was commonly observed in cases of gout, diabetes, chronic 
rheumatism, several forms of nephritis, scurvy, chlorosis, anemia, 
leukemia, and pregnancy. Also in disorders of the central nervous 
system and following the administration of mercury, lead, and iodin." 

Rhein states that the gingivitis produced by each of these diseases 
has distinctive features which may even serve as diagnostic signs of 
the nature of the general malady. 

Talbot's experiments in the mercurialization of dogs (see p. 644) 
demonstrate that efforts upon the part of the pericementum to elimi- 
nate the bichlorid of mercury result in a non-septic pericementitis, 
exhibiting in its morbid anatomy the characteristic round-celled 
infiltration of inflammation. 

Black 1 has shown that a gingivitis produced by the systemic 
administration of potassium iodid may be proved to be caused by 
its elimination by the pericemental glands by test of the gingival 
secretion for the iodin reaction. 

It is quite reasonable to suppose that irritative substances origi- 
nating in the body and floating in the blood stream may act in like 
manner. This has been termed auto-intoxication. 

Irritation resulting from the administration of mercury, lead, and 
iodin, or from toxic substances absorbed from the intestines, is, of 
course, extrinsic intoxication, but acts in the same manner. 

It has been claimed by Hunter, Herschell, Goadby, W. B. Keyes, 
D. D. Smith, and others, that the toxins formed by oral fermenta- 
tions and the septic infection of the stomach, intestines, etc., arising 

1 American System of Dentistry. 



DEEPLY SEATED GINGIVITIS 685 

from the mouth are competent to excite a train of systemic dis- 
turbances ending in a general malnutrition. 

Certain accomplished cures of such states by constant oral pro- 
phylaxis lend plausibility if not certain proof to this argument. 
Still, the malnutrition, whatever its cause, oral or otherwise, may 
become a predisposition by lessening the resistance of the soft parts 
about the teeth to local irritants or add the irritation due to auto- 
intoxication. 

Talbot claims that interstitial gingivitis is largely due to auto- 
intoxication due to intestinal fermentation with production of by- 
products, notably indol, which, when absorbed, may or may not be 
eliminated through the eliminating organs — liver, kidneys, skin, and 
lungs — and that if these be insufficient to the task, retention occurs 
and even further disease of the organs themselves, especially the 
kidneys. Constipation aggravates the condition, if not producing 
it, by retention of fecal matter with which the poisons should be 
eliminated. The overstrain of the kidney in the endeavor to take 
up the work of the liver (when that is diseased) in elimination, 
produces renal inflammation and impairment of eliminative func- 
tion. 

The blood is surcharged with accumulated poisons, the heart and 
arteries degenerate, and cardiac hypertrophy and arteriosclerosis 
are produced. Blood pressure is increased and end artery and nerve 
degeneration occur, in the brain, eye, alveolar process, pulp, etc., 
being noticeable first in the gums. He draws attention to the transi- 
tory nature of the alveolar process and the inability of the arteries 
to expand, as in soft tissues, and that poisonous products settle in 
the end arteries, and points out that gingivitis is a natural result 
of these conditions. The demonstration of infarction in the pulp 
due to systemic conditions, even in the young, has been made by 
Hopewell-Smith, and also indicates end-artery strain. 

Talbot regards indican, the absorbed product of indol in the 
intestine due to putrefaction and which is found in the urine, as the 
excitant of gingivitis in intestinal fermentation (auto-intoxication) 
and the general acidosis, as indicated either by an excess of acidity, 
in the urine or a deficiency therein, as excitant in various conditions 
of malnutrition. 

The excess of acidity above 40° in the urine indicates excessively 
imperfect oxidation, while defective acidity (below 30°) indicates 
insufficiency of renal elimination. In both cases systemic acidosis is 
the condition. (See p. 103, etc.) 

Diagnosis of Systemic Causes. — The diagnosis of systemic cause 
by malnutritional conditions involves almost the entire range of 



686 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 

medical diagnosis, a subject obviously beyond the scope of this 
work. If local causes do not explain the oral pathological condi- 
tion it is well to refer the patient to a competent medical diagnos- 
tician for examination and treatment. Urinalysis or salivary analysis 
may, however, be made by either the dentist or a specialist in that 
work, and together with symptoms some information may be gained. 
Talbot directs that twenty-four-hour urine should be obatined and 
the following points looked for. 1 

Amount. — This should be about forty ounces. 

Specific Gravity. — If high, it indicates an increased proportion of 
solids per ounce. 

Degree of Acidity. — If above 40° it indicates acidosis by imperfect 
oxidation; if below 30° it indicates renal insufficiency and retention 
in blood of acid products. 

Indican. — If present, it always indicates intestinal fermentation. 

Albumin. — Not of certain origin. 

Hyalin Casts. — If bloody, they indicate renal inflammation. 

Compound Hyalin and Coarsely Granular Casts and Waxy and Amyloid 
Casts. — Indicate changes in structure of kidney. 

Symptoms. — Headache, loss of appetite, loss of memory, irrita- 
bility, biliousness, fatigue, muscle soreness, hypochondriasis, in- 
somnia, vertigo, muddy complexion, tinnitus aurium, general ner- 
vousness, cold extremities, impotence, leg cramps, twitching of 
muscles, neurasthenia, pruritus, acne, urticaria, arteriosclerosis, gout, 
rheumatism, Bright's disease, diabetes, uric acid diathesis, nervous 
disorders, asthma, anemia, lethargy, stupor, insanity, etc., are 
symptoms which, in part, may develop from the auto-intoxication 
by the toxins and acidosis. (See General Malnutrition.) 

Unnatural odor of the breath, armpits, and thighs indicate an 
effort of the lungs and skin at elimination. 2 

Lead poisoning occurs in those using white lead, as painters. The 
occupation together with paralysis of the extensors as in wrist or 
foot-drop, tremors, and peripheral anaesthesia from toxic peripheral 
neuritis and the blue lead line upon the gum are diagnostic points 
with which mercurial symptoms of like character may be confused 
through urinalysis for lead; the history and occupation clear it up. 

In mercurial poisoning the occupation, history of drug adminis- 
tration, salivation, enlarged tongue, general pericementitis or gingi- 
vitis, urinalysis for mercury, will clear the diagnosis as against 
that of lead poisoning. 

1 Interstitial Gingivitis due to Auto-intoxication, Journal American Medical Asso- 
ciation and Dental Digest, 1906. 

2 Talbot. 



DEEPLY SEATED GINGIVITIS 687 

Pathology and Morbid Anatomy. — The local or systemic causes 
produce direct inflammation; the bloodvessels become overful, and 
waste products collected in the end arteries produce local degenera- 
tion, diapedesis of leukocytes into the interstitial submucous gum 
tissue occurs, and the spaces are filled with inflammatory exudate. 
The papillae become enlarged and the epithelial layer undergoes an 
increase in formation of cells (hyperplasia). The gum in consequence 
of these changes becomes swollen, its color deepened, and it bleeds 
readily. 

Fig. 612 Fig. 613 Fig. 614 





Resorption of alveolar process due to interstitial gingivitis, caused by marginal irri- 
tation from excessive filling material. (Radiographs by Price.) 



If the process be advanced the alveolar process is involved. 

After a time the effects of continued low-grade inflammation are 
expressed in resorption of bone or cementum, or both, or hyper- 
trophy of bone or cementum, or both, as the two processes may be 
in evidence at the same time. 

Talbot describes several forms of bone resorption occurring in 
interstitial gingivitis : 

(a) Lacunar resorption carried on by the osteoclasts normally 
lying upon the surface of the bone. Under irritation they increase 
in number and excavate irregular bays in the bone (Howship's 
lacunse). These are then deepened and widened, destroying areas 
of bone. (See p. 146.) 

(6) Perforating canal resorption beginning in the small canals 
normally perforating the trabecular of bone in various directions and 
transmitting the bloodvessels from one medullary space or Haver- 
sian canal to another (Volkmann's canals). The osteoclasts widen 
these, necessarily reducing the substance of the trabecule (Fig. 71). 

(c) Halisteresis ossium, beginning with a decalcification of masses 
qf the bone, the organic matrix being for a time undisturbed, but is 
later removed. This is a local expression of what may occur in other 
bones of the body in the condition known as osteomalacia (Fig. 74). 

According to Talbot, premature resorption of the alveolar margins, 



688 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 

either local or general, is due to this process, called by him alveolar 
osteomalacia, and occurs in pregnancy or senility, as a rule. 

He states that the decalcified bone may be recalcified after con- 
finement in pregnancy, but is never restored in senility. 
. A lesser degree of irritation may set the osteoblasts at work and 
cause the building up of the alveolar process, either as a restoration 
of resorbed bone or as an hypertrophy of either the alveolar process 
or the cementum of the root (hypercementosis) . 

Endarteritis obliterans is a thickening of the intima of an artery 
or capillary, due to chronic irritation, and causing a lessening of the 
lumen of the vessel, even to the point of obliteration of the capillaries. 

The blood flow is impeded and nutrition of cells impaired. Any 
cause of deeply seated inflammation may produce it. In all cases 
of chronic deeply seated gingivitis the bloodvessels are so diseased 
(Figs. 615 and 616). 



Fig. 615 



Fig. 616 




Fig. 615. — Longitudinal section of gingival border, showing round-cell inflamma- 
tion, due to mercury, and extending to the inner coat of the bloodvessel, and also 
plasma mast cells. From a dog. (Talbot.) 

Fig. 616. — Endarteritis obliterans: A, adventitia; E, elastic tissue between middle 
coat and intima; M, muscular coat; /, thickened intima. (Talbot, after Kaufmann.) 



Local Treatment. — The treatment must be directed to the removal 
of the underlying cause. All local causes must be removed and the 
teeth put into physiological use as far as possible. This includes 
the removal of causes of malocclusion or overuse; of the crowding of 
food between teeth, the removal of local mechanical irritants and 
infective agents. The local treatment in general is that employed 



DEEPLY SEATED GINGIVITIS 689 

for marginal gingivitis or for pyorrhea alveolaris. (See p. 677; also 
Pyorrhea Alveolaris.) 

Systemic Treatment. — This, of course, depends upon the systemic 
condition and its causes, but if due to torpid biliary function or 
defective elimination with consequent retention of body products, 
the restoration of the eliminative function should be aimed at. In 
intestinal auto-intoxication impacted fecal matter should be removed 
by repeated injections, if necessary, of warm water, and the bowels 
be kept clear by flushing with soap and water once or twice a week. 
The massage of the abdomen restores the tonicity of the bowels. 
The bile function should be restored, and the bile be increased in 
flow by calomel and soda, tV to £ gr., every hour until 1 grain is 
taken; to be followed by a saline laxative (as Seidlitz powder); or 
podophyllin, tV to f gr., up to J gr., may be given instead of calomel. 

Talbot 1 also uses* 

1$ — Aloin J gr. 

Strychnin sulphate jj gr. 

Extract of belladonna j gr. 

Pulv. ipecac jq gr. — M. 

Take at bedtime and follow with a saline cathartic next morning. 
If the stools remain unhealthy, administer each two to four hours 2 
to 5 grs. of compound lime, soda and zinc carbolate until the stools 
are healthy. 

To continue the stimulation of the liver administer bilin tV to 
J gr. four or five times a day. 

The urine should be examined for evidence of established disease, 
and if this be found the patient referred to a general practitioner. 
(See General Malnutrition.) If found only symptomatic of hepatic 
or renal insufficiency and nutritional disorder, the amount of urine 
should be increased to 40 ounces by the drinking of 3 pints of water 
(including table beverages) per day, which will aid bowel and renal 
elimination and flush tissues of accumulations, including retained 
acids. If the urine be abnormally acid (above 40°) administer 
3-gr. tablet of lithia, sodium bicarbonate, or sodium chlorid in a glass 
of water four times a day. Hot or Turkish baths keep the skin 
free for eliminative function. Well-apportioned rest and exercise 
and moderate eating of proper nutritious food are indicated. (See 
pp. 97 and 105.) When organic disease is present the treatment 
should be relegated to the medical practitioner. 

1 Therapeutics and Treatment of Intestitial Gingivitis, Dental Digest, 1906. 
44 . 



690 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 

MARGINAL ATROPHY OF THE GUMS. 

In advanced age there exists often a tendency of the gums to 
shrink evenly away from the enamel, exposing the cementum. Hope- 
well-Smith describes this as accompanied by fibroid degeneration 
of the pericementum (which see), and regards the latter as a purely 
senile change. 

It may be noted upon the buccal side only of a denture, and be 
due to vigorous brushing. 

It is also seen localized at cervices next to a space from which a 

tooth has been extracted. In one case the editor saw a slightly 

hypertrophied gum distinctly overlapping a cavity margin drawn 

back one-eighth inch within a month as the result of extraction of the 

adjoining root. 

Fig. 617 




Recession of gum in senility; beginning decalcification of cementum; alveolar resorp- 
tion after extraction. (Philadelphia Dental College Museum.) 

Apart from senile changes, and possibly even including them, 
these effects seem to be the result of an overstimulation of the gums 
resulting in atrophy. It may be that collections upon the teeth 
are in some degree responsible. The gums have, for the most part, 
a healthy look, but are in a condition predisposed to pyorrhea 
alveolaris. 

Treatment. — If localized and the restoration of the gum be desir- 
able, Harlan's method may be tried. 1 (1) Cleanse the exposed 

1 Dental Cosmos, 1906, p. 927, and 1907, p. 598. 



MARGINAL ATROPHY OF THE GUMS 691 

tooth surface and slightly roughen it near the gum margin. (2) 
Dissect away the gum from the root to about one-quarter inch in 
depth, wiping the blood away carefully with mouth open until 
hemorrhage ceases spontaneously, or check with adrenalin solution. 
(3) Make three incisions into and through the gum tissue. (4) 
When bleeding has almost ceased fill the cuts with dried zinc iodid, 
allowing the blood to liquefy it so that it may be carried around 
the gum margin. This creates a profound irritation, which should 
not be disturbed. (5) The patient should use a mild antacid anti- 
septic wash, as of sodium bicarbonate or milk of magnesia. (6) Re- 
peat three or four times at intervals of three or four weeks, with 
cuts in a new location. (7) Use silk or pure silver ligatures around 
the teeth under the gum for further irritation. (8) To allay over- 
irritation paint with 1 part adrenalin and 3 parts compound tincture 
of iodin once in three days. 

Harlan states that a long time may be required in some cases. It 
should not be attempted over a gold filling, but an unglazed porcelain 
may be covered, though no attachment will exist. The principle 
involved is that of coaxing the gum into adherence with the roughened 
root, and the filling in of the cut with scar tissue. 

As a wash use: 

]$ — Hydronaphthol gr. xx 

Oil eucalyptus TUx 

Oil cassia Tt\x 

Alcohol f 3 iij 

Distilled water f5xiij — M. 

Sig. — Use freely five or six times daily, diluted, if necessary, with more water. 

The gums should not be brushed for several days after operating. 
Avoid insoluble dentifrices. If this treatment be considered inad- 
visable the appearance in a given case may be improved by the 
use of a pink porcelain inlay. 

For general recession due to osteomalacia the general acidosis 
may be treated. 



CHAPTER XXIII. 
SALIVARY AND SERUMAL CALCULUS. 

Calculi are more or less hard concretions found in varying situa- 
tions and composed of inorganic and organic matter combined in an 
unknown manner. 

As related to the teeth, calculi arise from the following recognized 
sources : 

1. Obviously from the saliva, and deposited in situations which 
clearly indicate its source, salivary calculus (or ptyalogenic calculus 
— Peirce). 

2. From the serum of the blood deposited at some point along the 
side of the root between the gum margin and the apex of the root, 
and called serumal calculus (Black), or sanguinary calculus (Inger- 
soll). Of this there are several varieties: 

(a) That associated with a probable fermentation and an altered 
secretion from the gum margin, and known as subgingival calculus. 

(b) That occurring in situations in which a chronic pus flow is 
found, whether apical or subgingival, and which may be called 
pyogenic calculus. 

(c) That found upon the roots of teeth at a point to which saliva 
has no access and over which pus does not flow, and which is there- 
fore deposited by the lymph derived from the blood, and to which 
the appellation hematogenic calculus (Peirce) is applicable. 

In this class Kirk found two varieties resulting from pericemental 
inflammation: (1) Subpericemental deposits, and (2) intraperice- 
mental deposits. 1 

These several names will be adhered to in further descriptions as 
having definite significance. 

SALIVARY CALCULUS. 

Definition. — Salivary or ptyalogenic calculi are hard formations 
composed of salts of the saliva which have been deposited or precipi- 
tated and combined in an unknown manner with organic substances, 
probably mucin or globulin. 

1 Dental Cosmos, 1905. 

(692) 



SALIVARY CALCULUS 



693 



Occurrence. — They are found upon the surfaces of the teeth, 
notably in situations opposite the mouths of the salivary glands, in 
the ducts of the muciparous salivary glands (sublingual and sub- 
maxillary), and upon artificial dentures. A photograph of a plate 
containing an enormous mass of calculus, the result of seven years' 
accumulation, is shown in Fig. 618. The teeth are occasionally 
buried in it. The editor extracted three lower incisors which had 
been wired together, and were absolutely covered from the neck to 
the apex by calculus. 

Varieties. — Clinically two distinct varieties of salivary calculus are 
recognizable: (1) The soft, friable, whitish yellow deposits found 
chiefly upon the buccal surfaces 

of the upper molars and upon FlG - 618 

the lingual surfaces of the lower 
anterior teeth; (2) dark-colored 
and hard deposits found more 
frequently in the latter situation, 
less frequently in the former. 

Origin of Salivary Calculus. — 
The origin of salivary calculus 
may be studied from several 
standpoints: (1) The formation 
of calculi in other parts of the 
body; (2) an analysis of saliva 
and salivary calculi; (3) extra- 
oral experiments upon saliva 
with a view to the formation 
of salivary calculus extra-orally; 

(4) the changes observed clinically in salivary calculus during its 
deposition. 

Ziegler 1 states that all free concretions have an organic basis or 
nucleus (inspissated feces, vegetable material, epithelial scales, 
mucus, etc.). 

As to cholesterin gallstones, he states that if the cholesterin be 
dissolved out by ether, a yellowish organic matrix remains which 
retains the form of the stone and presents upon examination radiating 
spaces formerly occupied by the crystals. He describes the forma- 
tion of the gallstone as an infiltration or incrustation of degenerated 
organic matter (epithelial scales, etc.) with cholesterin, bile pigment, 
etc., to which, after a nucleus is formed, other portions are added in 
like manner. 




Salivary calculus attached to a lower 
partial plate worn seven years without 
removal. Shows form of sublingual 
space. Practice of Dr. Ford, Toulouse, 
France. (Specimen in possession of 
Philadelphia Academy of Stomatology.) 



General Pathology. 



694 SALIVARY AND SERUMAL CALCULUS 

Of urinary calculi he states that Ebstein has shown an organic 
substance albuminous in nature to be left after dissolving out the 
various salts. 

In stratified calculi this stroma also shows stratification. Such a 
stroma may be seen after decalcification of a bit of salivary calculus. 

Analysis of salivary calculus shows it to be composed of about 22 
per cent, of water and organic matter as the portion removable by 
burning the calculus, and about 78 per cent, inorganic matter as the 
portion removable by decalcification with acids. 

Following are the analyses of salivary calculus by Stevenson and 
Schehevetskey , respectively i 1 

Soft tartar Hard tartar on 

on molars. lower incisors. 

Water and organic matter 21.48 17.51 

Magnesium phosphate 1.31 1.31 

Calcium phosphate with a little carbonate and 

trace of fluorid 77.21 81.18 

100.00 100.00 

Water and organic matter 22 . 07 

Magnesium phosphate 1 . 07 

Calcium phosphate . 67.18 

Calcium carbonate 8.13 

Calcium fluorid 1 . 55 

100.00 

These observers are practically agreed upon the substances present 
in calculus as mainly calcium phosphate with some calcium carbonate, 
calcium fluorid, and magnesium phosphate combined with organic 
matter. 

Talbot furnishes the following analysis of serumal calculus by 
J. H. Salisbury: 2 

Water and organic matter 32 . 24 

Magnesium phosphate 0.98 

Calcium phosphate 63 . 08 

Calcium carbonate 3.70 

100.00 

To these Kirk 3 adds ammoniomagnesium phosphate as a product 
of putrefaction. 

According to Mitscherlich, 4 parotid saliva contains globulin, but 
no mucin, and contains calcium carbonate; calcium phosphate being 
present in but minute amount. The submaxillary saliva contains a 
large amount of mucin, which gives to mixed saliva its viscid nature. 

1 Talbot. Interstitial Gingivitis. 2 Ibid. 

3 Dental Cosmos, 1905, p. 752. 

4 Halliburton. Physiological and Pathological Chemistry. 



SALIVARY CALCULUS 695 

Analyses of submaxillary saliva and mixed saliva by Bidder and 
Schmidt gave the following results: 

Submaxillary Saliva. 



Water . . . 




. . 991.45 


Organic matter . 




2.89 




Calcium chloric! \ 
Sodium chlorid / ' 


. . 4.50 


Inorganic matter - 


Calcium carbonate 
Calcium phosphate > . 
Magnesium phosphate J 


. . 1.16 




1000.00 


Water . . . 


Mixed Saliva. 


995.16 


Organic matter . > 


f Epithelium 

i Soluble organic matter 


. . 1 . 62 
. . 1.34 


Inorganic matter • 


f Potassium sulphocyanid 
Sodium, calcium, and magnesium 
Sodium and potassium chlorid 


. . 0.06 

phosphate 0.98 

. . 0.84 




1000.00 



That an error of experiment or estimation exists in these analyses 
is shown by the fact that calcium carbonate is not mentioned as 
existing in mixed saliva, while it exists in submaxillary saliva; this 
is a physical impossibility. 

It is presumptive, however, that calcium carbonate has not been 
specially estimated. 

If a bit of calculus be dried and then burned at a red heat, the 
organic matter present will burn out, the calculus retaining its form. 
If a similar bit be subjected to dilute acid (1 per cent, nitric) the 
inorganic matter will be removed, the calculus will float to the top 
of the liquid, and, after a time, remain as a light stroma of nearly 
the original form of the piece. 

If a bit of calculus be transversely ground, it is seen under a low- 
power lens to present a laminated appearance — i. e., it has been 
deposited in layers representing periods of activity. The under 
surface of the calculus shows a concentric formation. Beneath the 
mass a nidus of darker calculus may be found, and if section of 
extensive calculi be made the greenish deposits may be seen scattered 
through the mass. Black has noted the presence of urates in nearly 
all specimens examined by the murexid test. Foreign bodies are 
sometimes entangled in the mass. Peirce recorded a case in which 
a small clasp plate was securely fastened to the teeth, and the patient 
denied possession of such a substitute. 

In some cases extensive salivary deposits are found associated 
with highly offensive odors — i. e., putrefaction of the organic matter 



696 SALIVARY AND SERUM AL CALCULUS 

occurs as a part of the process — indeed, bacteria are constantly 
associated with the mass and may furnish their quota of the organic 
matter. Extraneous matters, such as tobacco smoke or other pig- 
ments, cause discoloration of the mass. With data relative to the 
physical and chemical analysis of calculi, the mode of calculus forma- 
tion may be studied. It will be noted that the necessary elements 
of calculus formation are supplied by the saliva and food debris — 
?'. e., an organic basis is furnished in which calcium salts may be 
entangled, precipitated, or chemically combined. 

If a test-tube be filled with saliva and allowed to remain at rest 
for several days, a flocculent, light yellow precipitate will be noted 
at the bottom of the tube. If the supernatant fluid be drawn off 
with a pipette and the precipitate be allowed to dry, it will be found 
possessed of the chief characteristics of calculus — hardness, friability, 
a light yellow color, tenacity of adherence to objects with which it 

is in contact, and capability of 

,__£ IG - 619 analvsis into organic matter and 

S | • J . u s 

inorganic salts. 

The blood contains about 0.8 
per cent, of inorganic salts, includ- 
ing those found in salivary calculi, 
and a certain percentage of them 
is also found in the blood cor- 
puscles. They probably, there- 
A, nidus; B, calculus. fore, exist in body cells in some 

proportion. 
The salts are also taken into the body in the form of food. Their 
appearance in the various excretions and secretions of the body is to 
be regarded as in all probability an effort upon the part of the system 
to eliminate a superabundance of inorganic material from the body. 
The ingestion of quantities of animal or vegetable food rich in 
phosphates, or the excessive liberation of the phosphoric acid in 
malnutrition, may produce an excessive elimination of these in 
the excretions and cause a tendency to the production of calculi 
about the body. This condition, known as phosphaturia, is observed 
in certain nervous diseases, rachitis, osteomalacia, leukemia, gout, 
and rheumatism, 1 in which the phosphaturia is symptomatic of an 
excessive katabolism; also in intestinal disturbance resulting in 
imperfect assimilation of food. (See p. 111.) 

Whether taken in as food or liberated during metabolism it is 
probable, as pointed out by Talbot, that if one excretory organ fail 

1 Thompson. Practical Medicine. 





SALIVARY CALCULUS 697 

to perform its office in full degree another must take up its work. 
For this reason, in any bodily condition affecting elimination a 
superabundance of inorganic salts may appear in the blood and 
hence in the saliva, and, probably, in even the secretions from the 
gingival margins. 

That the deposit of calculus may have some dependence upon the 
superabundance of calcium salts in the saliva is evidenced by the 
fact that in young children but little calculus is deposited upon 
the teeth, though the oral fermentation is not lacking. The salts 
are needed in bone formation. . 

The Organic Factor of Calculus Formation. — Black 1 has argued 
from experiment that the organic basis is probably a colloidal agglu- 
tinating substance precipitated from saliva in the form of small 
oval or cylindrical globules, made up of a mulberry mass of fine 
globules. This substance he has called "agglutinin." This lodges 
upon solid objects and the minute particles of inorganic salts are 
precipitated into this. 

This substance is coagulated (white) at 200° F., but as freshly 
deposited is transparent, and has a soft, greasy, sticky feel. Micro- 
organisms multiply in it after a time, but at first it is free from 
them. Black has shown that this deposit precedes the infiltration 
by the salts. 

Black regards this substance as some product of faulty metab- 
olism, and as the determining factor in calculus formation rather 
than the presence of more or less calcium salts, and believes this to 
account for fluctuation in deposit. He found that the use once of 
Epsom salt as a cathartic would stop the accumulation of calculus 
for from a few days to several weeks, according to the condition of 
the patient. He regards the condition as not due to constipation, 
but rather due to the formation of a larger quantity of chyle than 
can be readily assimilated. In his own case he was able to limit 
calculus formation by reducing the intake of food and thorough 
mastication, and to bring it on at will by partaking heartily of rich 
foods. 2 The subject requires further investigation. 

Exposure of the roots of teeth, especially the lower anterior ones, 
favors the deposition of calculus, owing to the difficulty of brushing 
the surfaces. • 

1 Items of Interest, June, 1911. 

2 It is known that about one-third of calcium and other salts are eliminated in the 
intestinal secretion. It is therefore not certain from Black's experiments with Epsom 
salt whether the salts necessary for calculus formation are not so eliminated because 
of the stimulation of secretion from the surface of the swept and stimulated intestine. 
The fact that the quality of the chyle remained the same during the several weeks of 
lessened calculus formation seems rather to prove that retention of some organic 
or inorganic factor is of more importance than the quantity of chyle formed. Again, 
a lessened ration may reduce the quantity of the factors. 



G98 



SALIVARY AND SERUMAL CALCULUS 



That rest or relative quiescence of the saliva is favorable for the 
formation of calculus is shown by the fact that it occurs at points 
which are ordinarily not subjected to agitation — i. e., buccal surfaces 
of upper molars, lingual and labial surfaces of lower incisors. 

Adhesive precipitations of newly formed and very soft calculus 
form in these latter situations in the course of twenty-four hours. 
If not removed by brushing they harden and thicken. An unused 
side of a denture often accumulates calculus in greater degree than 
the side used for mastication. This does not occur, however, if the 
brush be used properly and equally vigorously upon both sides. 



Fig. 620 



Fig. 621 




Unclean necks of teeth, salivary calculus, 
and green stain. (Philadelphia Dental Col- 
lege Museum.) 



A, maxillary sinus ; B, duct of Steno ; 
C, parotid calculus; E, submaxillary 
gland. 



Burchard pointed out that' irritations of various natures about 
the teeth and gums may by reflex action cause secretions of fluid, 
abnormal in quantity and quality, from both the salivary glands and 
the buccal parietes (glands and gum margins) . It is more probable, 
however, that the systemic condition and uncleanliness, together 
with tooth form, is largely responsible. The editor has a patient 
who is abstemious, eats moderately, exercises indefatigably in the 
open air, and drinks water freely. During the golf season, when 
perspiration is free, he has somewhat less calculus, but always 



SALIVARY CALCULUS 



699 



has some at uncleansed spots. This appears within two weeks of 
prophylaxis. 

An increase of oral fermentation is commonly associated with an 
excess of calculus formation, but conditions of oral fermentation 
may be seen in which but little deposit occurs. The mouths of 
many children are examples of this. 

Fig. 622 
S.LC 




S.L.G.L 
C, calculus; S.L.C., sublingual cavity; S.L.GL., sublingual gland. 



Fig. 623 




Right side, abrasion from overuse; left side, deposits due to stagnation. 



, Calculi harden with age. It is commonly noted that soft calculus 
may be readily removed with a brush. Calculus deposited upon 
lower teeth within a week or two after a thorough cleansing may be 
scraped away as a cheesy mass; after a much longer time it comes 



700 



SALIVARY AND SERUMAL CALCULUS 



away as a hard scale. In very old deposits it may be exceedingly 
hard and quite firmly attached to the teeth. 

These clinical observations confirm the deduction that an infiltra- 
tion of calcium salts occurs in the organic stroma of the calculus, 
analogous to that occurring in dead or degenerative tissue throughout 
the body (calcareous infiltration or degeneration). It is probable 
that a firmer chemical combination of the organic and inorganic 
elements of the calculus occurs as time passes, density being thereby 
increased. The organic basis is evidently a precipitation of a col- 
loidal material, probably mucinous in character, upon the teeth, and 
into this the salts are precipitated. 

In the analyses furnished by Stevenson (p. 694) it will be seen 
that hardness is, in part at least, due to an increased proportion of 
inorganic elements. 



Fig. 624 



Fig. 625 





Section of a lower incisor, with a large 
deposit of salivary calculus impinging 
upon and causing inflammation of the 
gum. (Black.) 



Section of an upper molar with deposit 
of calculus on its buccal surface, causing 
inflammation and absorption of the gum 
and lower border of the peridental mem- 
brane and alveolar wall. (Black.) 



Theoretically, subgingival calculi, pyogenic calculi, and hemato- 
genic calculi formed within the unbroken pericementum may derive 
their organic material from the secretions or necrotic tissue of the 
part, and their inorganic material (largely phosphate of calcium, 
carbonate of calcium, and sodium biurate) from the serum of the 
blood (serumal calculus). In the case of simple subgingival calculus 
the saliva may play a part by furnishing the necessary calcium 
salts, as claimed by Peirce, but this does not seem to be absolutely 
proved, nor would it seem to be necessary; indeed, in certain cases 
of pyorrhea pockets located about lower incisors in which salivary 



SALIVARY CALCULUS 



701 



calculus might readily he deposited, and from which hoth salivary 
and serumal calculus has been thoroughly removed, the serumal 
calculus has again collected in quantity, while the salivary calculus 
has not been redeposited. 

Pathological Effects of Salivary Calculus. — In contact with the 
mucous membrane a salivary calculus excites first marginal gingivitis, 
and later deeply seated gingivitis and its effects. There is sometimes 
in this stage the wavy, gnawing, uneasy sensation, associated with 
mild inflammation, and the pulp being supplied with excess blood, 
becomes hyperemic and the teeth respond more readily to thermal 
stimuli. (See p. 470.) The gum margin is inflamed, and occasion- 
ally pyogenic organisms cause pus formation. The gum margin 
recedes and coincidently a resorption of the alveolar process is 
produced. More calculus is deposited and the process proceeds 
until much of the alveolar support is lost. Microorganisms no 
doubt aid in the process. 



Fig. 626 



Fig. 627 




Section illustration of a heavy deposit 
of salivary calculus on a lower incisor, 
with partial destruction of the alveolus 
of the tooth. (Black.) 




Sectional illustration of lower in- 
cisor, with deposit of salivary cal- 
culus less heavy than that shown in 
Fig. 626, but with greater destruc- 
tion of the alveolus. (Black.) 



The tooth is thus progressively loosened, first by inflammation, 
later by loss of alveolar process, moves about, and a resultant mechan- 
ical interstitial inflammation of the remaining pericementum occurs; 
as a result the membrane is thickened and the alveolar process 
partially resorbed (Fig. 624). As soon as the aveolar loss is con- 
siderable, infection usually occurs and suppuration may be grafted 
upon the results of mechanical irritation. Increased looseness occurs 
until the tooth drops out, unless mechanically held in place. 



702 



SALIVARY AND SERUMAL CALCULUS 



The entire process may occupy but a few years; in other cases 
the atrophy of the alveolar walls is very slow. I have recently seen 




George H. Cushing's scalers. The forms and general character of these 
scalers are well shown. All the instruments except No. 6 are intended to 
be used with the push stroke. Nos. 1 and 2 are especially intended for 
application to the posterior surfaces of lower incisors; they are also admir- 
ably adapted for removing calculus deposits below the gum between molars 
and bicuspids, and from the posterior surfaces of the last molars. No. 2 
can be passed quite to the extremity of most roots with less disturbance 
to the soft tissues than a thicker or more rigid instrument would cause. 
Nos. 3 and 4 are for removing deposits at and below the gum between the 
teeth, particularly the lower front teeth. They can also be easily used 
upon the sides of the roots of many teeth, being passed toward the apex 
of the root in a line nearly or quite parallel with that of the axes. No. 5 
is intended to be passed between the lower front teeth at or near the gum and 
then directly upward, to remove the deposits on the proximal surfaces. 
No. 6 is a hoe, and is intended to be passed quite to the apex of the roots, 
where a hoe is desired. 



a case like that shown in Fig. 626 on about eight 
lower teeth. The patient had not consulted a 
dentist for thirty years. 

Prognosis. — The prognosis of this condition 
depends upon the extent of alveolar atrophy. 
If the loss of support be not so extensive as to 
cause marked loosening of the tooth or teeth, 
the teeth may be retained for an indefinite period 
if they receive constant prophylaxis. If markedly 
loosened they must be splinted so as to render 
them firm. If left unsupported, the pericementum 
is certain to degenerate, owing to the increased 
mobility. The alveolar atrophy will continue, 
and probably infection of the degenerated perice- 
mentum occur. Redeposit is almost certain unless 
all morbid conditions are removed and extraordi- 
nary precautions be taken as regards cleanliness, which precautions 
are difficult to carry out without the aid of a dentist. 



Fig. 629 




Flat scaler. 



SALIVARY CALCULUS 




703 
Fig. 631 



E. C. Kirk's scalers with dentate ends, designed to cut into 
calculus as well as maintain the course of the scaler upon the 
root side. 



Fig. 632 



Fig. 633 



Fig. 634 






No. 3 Scaler. 



Fig. 635 



No. 11 Darby 
Perry scaler. 

Fig. 636 



5 6 

Pyorrhea scalers Nos. 5 and 
6, revised set. S. S. White 
Dental Mfg. Co.'s Catalogue. 
Intended for use between teeth 
as well as for pyorrhea. 

Fig. 637 




,No. 9 Darby-Perry No. 35 Darby-Perry Burton Lee Thorp' 
scaler. excavator. scalers. 



704 



SALIVARY AND SERUMAL CALCULUS 



Treatment. — The treatment may be divided under three heads: 
removal of deposits, correction of the effects of their presence, and 
prevention of their recurrence. The sole means of removing salivary 
calculi should be instrumental. 

It is frequently recommended that mineral or some of the organic 
acids be used to soften the deposits or facilitate their removal. 
Anyone having seen a case in which a solution of sulphuric acid 
has been used for this purpose needs no further warning against 
the application. Acid solutions will certainly soften the deposits, 



Fig. 638 



• 




I 11 (i h 

12 13 14- 15 



16 |l 




2 3 4- 

FRONT 

Smith scalers. 

but at the same time inevitably cause a roughening of the enamel 
of the teeth by a solution of the calcium salts. To be sure, the 
acid does affect the calculus more than it affects the enamel, but 
the roughened surfaces of the latter not only invite widespread 
deposits of fermentable material, but render certain the more exten- 
sive accumulations of calculi in the future. 1 After oral sterilization 



1 Recently a proprietary preparation was offered me for removal of stains with 
assurance by the maker that no injurious acid was present. I highly polished the 
labial of an extracted tooth and applied it for one minute. The enamel was dulled 
and roughened. The preparation was acid to litmus. Such preparations, if needed 
in extreme cases, should be used with great care. 



SALIVARY CALCULUS • 705 

the gross deposits may be removed by means of large, sickle-shaped 

sealers, nearly all used with a draw cut. The instruments should 
have sharp edges and be introduced beneath the deposits, so that 
the gum be not unnecessarily wounded. The scaling should be 
continued until every surface which can be cleaned by these instru- 
ments is perfectly smooth. 

For the approximal surfaces of the low T er anterior teeth the flat- 
bladed instruments should be used with the push cut, or that in 
Fig. 651 with the draw cut. Younger's pyorrhea scalers are very 
useful (Fig. 649). Thorpe's scalers are useful (Fig. 637.) 

For the removal of associated subgingival calculus not too deeply 
placed beneath the gum a No. 35 Darby-Perry excavator is of almost 
universal utility. It is used with the draw cut for the most part. 
A pair of them may be employed and made safe-sided by rounding 
one edge if desired, to avoid injury of the gum margin. The back 
of the instrument may be sharpened to an edge for a push cut. 
Smith's file scalers (Fig. 638) are useful for rubbing off calculus that 
can not be scaled off as a flake. All of the calculi visible, and all 

Fig. 639 



'""n /-'~N ( ; 



Moose-hide wheels. 

that can be detected by their roughness, are thoroughly detached 
and scraped away with instruments. The surfaces of the teeth 
are next cleansed with pumice made into a paste with glycerin to 
prevent spattering, and with a few drops of hydrogen dioxid for 
antisepsis; flavoring matter or cologne may be added. The paste 
is applied to the surfaces of the teeth with rubber cups, or Abbott's 
or Robinson's brush wheels, wmich are used to cleanse the labial, 
buccal, and such lingual faces of the teeth as they will reach (Figs. 
640 to 644). The gum should not be injured. When using brush 
wheels it is well to apply the brush to a point away from the gum 
and spread the bristles sgainst the tooth as it is carried toward the 
gum. The second brush in Fig. 640 is the best for the labial sur- 
face and lingual of bicuspids and molars, and the third one for the 
lingual of lower incisors. The lingual surfaces of upper and lower 
incisors are cleansed with moose-hide wheels and wheel brushes; a 
finishing bur 1 is useful in the removal of thinly distributed hard 

1 Guilford Lectures. 
45 ' 



706 



SALIVARY AND SERUMAL CALCULUS 



calculi on lingual and occlusal surfaces, especially in the mouths 
of smokers. 

The approximal surfaces of the teeth are cleansed with fine linen 
tape or flat floss silk charged with the pumice paste. More inac- 
cessible parts require the use of an orange-wood point mounted in 
a Jack porte-polisher (Fig. 645). It is advisable to repeat the 
polishing with precipitated chalk and the same carriers. When 
prophylaxis is frequent chalk is a sufficient abrasive except perhaps 
with the wood point. 

Fig. 640 

SF W 'IF ^ W 




I 



y 



Abbott brush wheels. 



Fig. 641 



Fig. 642 





After cleansing, the associated gingivitis should be reduced and 
the parts kept sterilized while healing by means of an antiseptic 
astringent mouth wash. (See Gingivitis.) 

If desired, the operation may be divided, the gross deposits and 
subgingival calculus being removed at the first sitting. After a few 
days' use of the mouth wash the stains and bacterial plaques upon 
the teeth and any overlooked deposits may be removed. Tincture 
of iodin painted over the teeth brings the deeper stains of the 
collection into prominence, as does also a solution of potassium 
permanganate. 

Register states that a forcible spray of 1 per cent, hydrogen dioxid 
used after the application of tincture of iodin will soften the stains 
and render them more readily removable. The iodin is also rather 
germicidal. 



SALIVARY CALCULUS 



707 



Prophylaxis. — The smoother the surfaces of the teeth are made, 
the longer the redeposition of calculi will be delayed. Black sug- 



Fig. 643 



Fig. 644 



Fig. 645 






gests the use of the ordinary chip syringe and plain 
water, a forcible stream being accurately used to 
wash away the agglutinin. As a means of calculus 
prevention it should be valuable. 

It is a wise measure to cleanse the teeth before 
any long series of operations is undertaken, and 
as a prophylactic measure in the combat with 
caries and pyorrhea alveolaris the operation 
should be frequently performed. Indeed, the 
teeth should be cleansed frequently, so that it 
may not be necessary to remove actual salivary 
calculus, except in those cases in which it col- 
lects with abnormal rapidity. A stick in a metal 
handle for self-prophylaxis is useful if the patient 
will use it. (See p. 442.) 

In cases of very rapid recurrence of salivary 
deposits, evidence of an associated systemic 
condition should be sought. In this direction 
sialosemeiology and urinalysis may develop data 
worthy of attention. The systemic condition, if 
recognizable, should receive appropriate treat- 
ment. If not recognizable, the method suggested 
by Black of reducing the quantity of food and 



Wm: 



Jack porte-polisher. 



708 



SALIVARY AND SERUMAL CALCULUS 



the thorough mastication of such as is taken, may be conjoined 
with the occasional use of Epsom salt, if further needed as sug- 
gested. (See p. 697. ) 

SUBGINGIVAL CALCULUS. 

By subgingival calculus is meant that form of deposit which 
occurs beneath the free gum margin and between it and the tooth. 
The deposits consist of small scales or granules, usually quite smooth 
and much darker (olive green) than salivary calculi (Fig. 646). 



Fig. 646 



rf*,\>% 



1 M^^&v 








A, subgingival calculus; B, receding 
pericementum. (Black.) 



Resorption of the septum of bone and 
recession of the gum between the central 
and lateral incisors, caused by deposits of 
serumal calculus under the gingiva?. 
(Black.) 



Composition.- — They consist mainly of calcium phosphate combined 
with undetermined organic substances. (See pp. 694 and 697.) 

Fig. 648 




The alveoli irreparably destroyed by calcic inflammation. (Black.) 



Cause and Pathology. — It is probable that some degree of marginal 
gum irritation first occurs, though many cases of an apparently 
healthy gum with a scale of calculus beneath it are seen. Whether 
the irritation arises through fermentations about the unclean necks 



SUBGINGIVAL CALCULUS 709 

of the teeth or as the result of an effort upon the part of the gum 
margin to eliminate waste products from the system is not absolutely 
certain. 

The theory most tenable is that uncleanliness exists; fermentation 
of the mixed marginal collection and altered gum secretion contain- 
ing a precipitable organic material, occurs, the gum secretion con- 
taining also calcium salts; these are precipitated, forming a calculus. 
Fig. 297 shows a calculus on an unerupted tooth root, showing that 
the blood contains the elements necessary for its formation under 
localized irritation. 

Talbot has shown that a natural pocket may exist at some aspect 
of the gingival space which is capable of harboring collections of 
foreign material. The normal gum margin closely approximates 
the tooth and has an apparent protective influence over the portion 
it covers. For some reason, such as a lack of normal friction or 
the presence of microbic plaques just above it, the gum may lose its 
normal tone and the calculus deposition be favored. Its secretion 
is also probably altered in quality. 

Effects and Symptoms. — The direct effects are exerted upon the gum 
margin. The mechanical irritation may cause the gum and alveolar 
process to undergo resorption, the calculus being exposed. 

At times this resorption is accompanied by evident marginal 
inflammation, at others the gum margin has a normal color, but the 
resorbing portion is sharply defined by a fine line (or crease) from 
the normal gum tissue, especially at the interdental septum. In a 
more advanced stage this demarked portion appears sunken or 
atrophied, and may have a sort of semihyalin redness characteristic 
of the inflammation. At times the gum margin appears everted 
(Fig. 647 a). If the deposit occur on only one side of a root the gum 
resorption may be confined to that side. 

The lingual root of an upper molar is often exposed for a con- 
siderable portion of its length by successive deposits of calculi. The 
same is true in other situations, notably upon the labial surface of a 
lower incisor. This might be called a form of marginal phagedenic 
gingivitis. 

If the deposit be generally distributed about the neck of the tooth 
the resorption is more equalized. 

In some cases the bifurcation of roots may be exposed and calculi 
deposit in that situation. 

« In some cases the gum margin becomes simply atonic or passively 
congested and is pushed away from the teeth by large masses of the 
calculus, which undergo lateral accretion. It appears as a flabby, 
thickened, loosened gum margin, which readily draws about the 



710 



SALIVARY AND SERUMAL CALCULUS 



necks of the teeth if the calculus be removed. I have noted this 
in cases of suboxidation with bluish lips, and in renal insufficiency. 



Fig. 649 






5 6 



7 8 




Fig. 650 




it II 

9 50 II 12 13 14 15 

Younger's new set of pyorrhea instruments. (Revised by Dr. Robert Good.) 

Fig. 651 




Tompkins' pyorrhea scalers. 



Finally, pyogenic infection may occur about the calculus and the 
symptoms of pyorrhea alveolaris be implanted. When this is estab- 
lished, calculi may be deposited farther up the side of the root. This 



HEMATOGENIC CALCULUS 711 

pathology often precedes the condition of pyorrhea alveolaris which 
may supervene if pyogenic organisms enter the area. 

Treatment. — The calculus should be removed by means of delicate 
scalers used with either the push or draw cut, as most convenient, 
after which astringent antiseptic mouth washes should be prescribed. 
The subsequent frequency of removal of causes by oral prophylaxis is 
of great importance. Figs. 649, 650, and 651 show convenient forms 
also useful for the deeper pyorrhea pockets. In most cases healing 
is spontaneous even without medication, but often the washes are 
of advantage. If pyorrhea be present on any tooth it is to be con- 
sidered separately. 

PYOGENIC CALCULUS. 

Pyogenic calculus is that form of serumal calculus which is deposited 
at parts of the tooth root over which pus more or less continually 
flows. Talbot has shown that pus is rich in calcium phosphate. 

In chronic apical abscess the root end may become encrusted with 
it, and in those cases in which apical abscess discharges along the 
pericemental tract it is common to find over the area fine granular 
deposits which vary in color from a light yellow to a reddish brown. 

The same is true of active pyorrhea pockets. 

This calculus prevents the healthy apposition of the gum tissue 
to the roots, probably because of its irritant and infective nature 
(Figs. 558 and 652). 

Treatment.— All such calculi should be removed by whatever 
means -possible, which may necessitate scraping the root end or 
its side, or even the amputation of the apical end of the root. In 
some cases 25 per cent, sulphuric acid or Tartasol may dissolve 
it. (See pp. 622 and 738.) 

HEMATOGENIC CALCULUS (Syn. SANGUINARY CALCULUS). 

This form of serumal calculus occurs in the so-called gouty peri- 
cementitis, a form of pericemental abscess. 

It may occur in the abscence of apical abscess or a primary pyorrhea 
alveolaris, and, therefore, at points not acted upon by saliva or pus; 
hence it must be deposited by the blood through the lymph. 

Miller 1 has offered satisfactory evidence of this in a description of 
a case of impacted cuspid well embedded in the bone, and not in 
any way exposed to either saliva or pus influence except that at a 

1 Dental Cosmos, August, 1901. 



712 SALIVARY AND SERUMAL CALCULUS 

point over the cusp the gum underwent suppuration for a short time. 
The crown had undergone resorption, showing local irritation, and 
an olive-green calculus had formed upon the middle third of the 
root. Cases of pericemental abscess have been noted opening 
upon the gum face and presenting dark green calculi upon the root 
in that situation (Fig. 297). (See Pericemental Abscess.) 

Peirce found in such deposits a proportion of sodium urate as 
shown by the murexid test and the cases associated with goutiness 
of the patient. 

While such deposits may not cause immediate irritation, they may 
in time excite inflammation and necrosis of tissue, resulting in a 
discharge of glairy material representative of the condition. This 
form of dental disease will be further discussed. 



CHAPTER XXIV. 
PYORRHEA ALVEOLARIS. 

General Considerations. — The term pyorrhea alveolaris means a 
flow of pus from a pus pocket located between the root of the tooth 
and the alveolar wall at the lateral aspect of the root. Apical and 
lateral abscess from gangrenous pulp or perforation are excluded. The 
alveolar wall may be more or less intact and either be exposed and 
necrotic or, as more generally the case, be still covered with its 
internal periosteum, which is the remains of the pericementum. 
In some cases the bone has disappeared and the gum tissue forms the 
outer covering. Pyorrhea alveolaris always involves the considera- 
tion of marginal and deeply seated gingivitis, but these need not 
necessarily be pyorrhea. It is therefore somewhat difficult to differ- 
entiate from gingivitis proper, as any form of gingivitis may later 
assume the characteristics of pyorrhea owing to infection. 

In a general way pyorrhea alveolaris may be diagnosticated when 
there is a progressive gum pocket formed at the expense of the 
lateral portion of the pericementum, and the tooth becomes pro- 
gressively loosened. Usually calculi and a pus flow are found, but 
in some cases neither are much in evidence. 

The disease ceases spontaneously with the loss of the teeth, though 
the alveolar process is further resorbed as after any extraction. 

Causes. — It seems that anything which may induce a gingivitis 
may initiate the process when infection is added of a character that 
will destroy the pericementum and produce the pocket at its expense. 
Therefore the causes of gingivitis or even of non-septic pericementitis 
are the primary causes of pyorrhea alveolaris (see pp. 665, 674, and 
682, etc.). 

The gingivitis itself is the proximate predisposing cause and the 
specific infection is the proximate exciting cause. It is obvious that 
these are difficult of exact differentiation, i. e., it is difficult to say 
when gingivitis ceases to be such and becomes a pyorrhea, but when 
the pocket is established the case may practically be called a pyor- 
rhea, and is treated as such. From a prophylactic standpoint it is 
wise to remove all causes of gingivitis as it is apt to lead to a pyorrhea. 

The causes of marginal gingivitis are mostly obvious and have 
been discussed. (See p. 674.) The causes of deeply seated gingivitis 
apart from pyorrhea are more obscure, but, as stated in the dis- 

(713) 



714 PYORRHEA ALVEOLARIS 

cussion (p. 682), are either the more deeply acting causes of marginal 
gingivitis or are due to local or systemic causes which produce a 
more or less profound pericementitis or gingivitis apart from the 
alveolar pockets, and which have a tendency to cause inflammatory 
degeneration of the soft tissues and to produce a resorption of the 
bony tissue, thus predisposing the soft tissues to the local action of 
bacteria, or, in other words, lessening their resistance to bacteria. 

Aside from inflammatory conditions actually produced by sys- 
temic conditions, the pericementum may be influenced by a lack of 
proper nutrition, as in anemia or neurasthenia or some form of 
systemic drain, as peripheral nutrition is evidently lessened in such 
states, and tissues seem more subject to infection. The opsonic 
index is probably lowered. (See p. 62.) 

Investigations as to cause have proved uncertain in so far as the 
determination of a specific bacterium is concerned. 

Galippe and Malassez, Miller, Black, Talbot, Goadby, Younger, 
Cook, and others have all failed to definitely isolate such a specific 
bacterium. The closest approach to a demonstration yet made was 
the determination by Kirk of the presence of a pure culture of the 
Diplococcus pneumoniae in a few cases of freshly opened pericemental 
abscesses (which see). 

The investigations of Goadby, however, do not confirm this as a 
cause of pyorrhea alveolaris in general, but rather point to the prob- 
ability that the cause may be found among other oral bacteria, 
possibly thread forms or some of the blastomycetes. Talbot believes 
the ordinary pyogenic cocci to be the cause of the pus production. 

Recently, M. T. Barrett, 1 working with Allen J. Smith, M.D., 
has found in the pus of 46 straight cases of pyorrhea actively motile 
endamcebse (probably Prowazek's endamceba buccalis (Barrett)). 
Of ten apparently healthy mouths used as controls close examination 
revealed three with pockets with endamcebse in the contents and 
seven without pockets or endamcebse. The local treatment with 
an amcebacide (emetin hydrochlorid, J to 1 per cent., in normal 
saline solution was effective on several successive days. He refers 
to a flagellate protozoon and a ciliated one as found occasionally. 
Whether this is the exciting cause of pyorrhea, Barrett has not yet 
definitely claimed. Chiavaro 2 also found the endamceba buccalis, 
but regards it as non-pathogenic. 

Curtis 3 believes obstinate cases of the disease to be either caused 
by or aggravated by tertiary syphilis. He bases his belief upon 
observations of fresh blood which, he states, upon the authority of 
Dr. Robert L. Watkins (New York City), contains syphilitic spores. 

1 Dental Cosmos, August, 1914. 

2 Ibid., September, 1914. 3 Ibid., 1901. 



GENERAL CONSIDERATIONS 715 

"Egg-skin" eschar is the oral pathognomonic sign. 

According to Curtis, the local infection in nearly all cases is of 
so mixed a type as to render it at present uncertain whether the 
liquefaction of the peridental membrane, etc., is due directly to 
the pyogenic organisms present in the pus formed or to other oral 
bacteria of uncultivable type which may initiate the process, after 
which pyogenic organisms may enter and form pus. The fact that 
pyorrhea alveolaris is seldom found fully established before thirty 
years of age, but is common after that period, and that it occa- 
sionally occurs in youth or even in childhood associated with some 
pronounced systemic state or disease, strongly indicates a systemic 
factor in the more pronounced forms of the disease. 

The type of teeth affected is usually that of the narrow-necked 
variety in which the angle formed by the gum and tooth is less 
accessible to the brush and friction of mastication. This leads both 
to formations of calculus and to the retention of infective material. 

In brief, it may be stated that the infectious nature of pyorrhea 
alveolaris is becoming more established though not yet fully scien- 
tifically proved, and that the causes probably require a local predis- 
position for their action, though it may be that continued infection 
is a sufficient cause. This local predisposition may be the outcome 
of local sources of irritation and degeneration alone or be produced 
by waste products floating in the blood stream, etc., or by a lack of 
nutrition due to general causes. Clinically in support of a local 
origin it may be observed that oral conditions leading up to pyorrhea 
are seen existing for years previous to a fully established and active 
condition. The presence of such a state therefore must not lead 
one hastily to assume that it is of necessity a disease of systemic 
origin, and at present the systemic sequels of pyorrhea seem of more 
importance than its possible systemic origin. In observing mouths 
at all times one should look ahead from all forms of gingivitis or causes 
liable to produce it to a possible future pyorrhea and take measures 
to prevent it. (See pp. 665, 674, and 682.) 

Clinically, fully established cases of pyorrhea alveolaris may be 
divided into three classes: (1) Cases associated with a primary 
gingivitis and with the formation of hard, scaly, dark, annular 
calculi beneath the gum margin (subgingival calculus), the pockets 
not usually extending far beyond the deposits; (2) cases beginning 
with a marginal gingivitis and apparently not dependent upon the 
association with calculus, though frequently complicated by it; 
(3) cases having an apparent origin at some point between the 
gingival margin and the apical tissue, the gingival margin at first 
being apparently intact. 



716 PYORRHEA ALVEOLARIS 

It is probable that the infecting agents in these types differ in 
their nature, or that in the event that they may be proved to have 
a similar origin the tissues react differently to them, either partially 
resisting them, forming calculus as a result of the irritation, or 
rapidly giving way to them, permitting a deep action. 

In the abscence of known causes the conditions may be divided 
according to their clinical expressions. 

In the consideration a pus flow due to apical abscess, lateral abscess 
upon a perforation, or that due to obvious salivary calculus (for 
these, see under proper headings), also simple gingivitis or deeply 
seated gingivitis, not resulting in the clinical feature of pyorrhea as 
defined, are excluded. 

PYORRHEA AVEOLARIS BEGINNING AS A MARGINAL GINGI- 
VITIS AND ASSOCIATED WITH SUBGINGIVAL CALCULUS. 

Causes. — The causes of this condition are those predisposing and 
exciting causes of marginal gingivitis which have been described. 
(See p. 674.) Several local factors have to be considered in this 
connection: (1) The marginal infection; (2) the irritative effects of 
any calculus that may be formed; (3) the deep infection by pyogenic 
organisms; (4) the modification of the progress of the disease by the 
attendant loosening of the teeth and death of the pulp. 

Clinical History, Pathology, and Symptoms. — There is usually an 
unclean condition of the teeth; infection exists either in tenacious 
films of bacteria attached to the necks of the teeth and requiring 
reasonably close observation for their detection, or in masses of 
detritus readily noticeable. Subgingival calculus is, as a rule, 
obviously present (Fig. 657). 

The gum margin may be atrophied or be inflamed; or it may have 
a fairly normal appearance. When the gum margin is pressed upon, 
pus may be squeezed out in variable quantity. . 

It is assumed that the local infection brings about the deposit of 
mucous exudates rich in calcium salts at a point beneath the gum 
margin, and that formation of subgingival calculus occurs, followed 
by pyogenic infection and pus formation. 

The gum may now be resorbed either with apparently normal 
bulk or the margin may be everted and thickened into a cord-like 
margin which is either of normal color or inflamed; the shrinkage 
of the gum causes the exposure of the calculus (Fig. 646). In this 
manner the bifurcations of the roots may be uncovered and calculi 
be deposited in that situation. The resorption may only be con- 
fined to one side of a root and be the result of several successive 



PYORRHEA M.\E()L.\R1 s AS A MARGINAL GINGIVITIS 717 

depositions which may remain when the gum recedes, or which may 
be removed and again be deposited. In this way the side of the root 
may be exposed nearly to, and in some cases quite to, the apex. 

Fig. 652 




fit 



msm 



Serumal calculus, showing stalactite-like formations. (Talbot.) 

The destruction of the tissues may assume several forms. In 
certain mouths, especially in neurasthenic and anemic patients, a 
viscous material may accumulate upon the necks of teeth or exposed 

Fig. 653 




Destruction of pericementum, bone, and gum over buccal root of a molar. 



roots; and the pericementum, bone, and gum may rapidly inflame 
and disappear, leaving the roots exposed to collect more of the 
material, while pus may not be much in evidence. 



718 PYORRHEA ALVEOLARIS 

The resorption may occur as shown in Fig. 654, or the gum may 
be split and the destruction follow the length of the root on one side 
only until even the apex is reached (Fig. 653). 

The tooth may be loose or firmly attached by the remainder of the 
pericementum. This is especially true of" those teeth having very 
narrow necks, in which the roots describe a prominent curve just 
above the cervix. 

Fig. 654 




Resorption of gum over palatal root of an upper molar, associated with but trifling 
deposit of calculus, but the root is covered with a viscid deposit. Aged thirty-two 
years. Patient neurasthenic and of tuberculous diathesis. Condition in 1904. Tooth 
lost in 1907. In 1912 several other teeth were lost. In 1914 several more have gone. 

Fig. 654 is a model of the lingual side of the right upper teeth 
undergoing the former process. The left upper posterior teeth and 
the lower incisors have also been lingually affected. There is but 
little calculus, but the viscous material is quite abundant, black 
stain is present, and dental caries is rife. The patient has been 
anemic and neurasthenic for years, and one lower molar has been 
removed for resorption of the apices of the roots associated with 
looseness. Many teeth have been lost. The patient is unable to 
perform an exact dental toilet and does not employ the dentist as 
she should. 

In such cases the pus pocket may not be deep and the pus formed 
may readily be washed away. Such cases present some resemblance 
to simple gingivitis and might be so classed if there were no pus flow. 
Instead of this the pericementum may be progressively destroyed 
by suppuration and the gum margin remain practically intact. In 
these cases the pus flow is more abundant, a deep pocket is formed, 
extending a third or even two-thirds or more of the length of the 
root (Fig. 655). It is common to find beads of calculus deposited 
along the side of the root and presumably of serumal origin. (See p. 
708.) The cementum being deprived of nutrition, its minute nutri- 
tional openings or openings containing fibers harbor bacteria. 

These inflammatory disturbances necessarily involve deeply 
seated gingivitis or infiltration of leukocytes into the interstitial 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 719 

connective tissue of the gum. As pointed out by Talbot, resorption 
of various kinds and at times constructive changes accompany such 
an inflammation. (See Deeply Seated Gingivitis.) Endarteritis is 
also noted. These results are noted in connection with this variety 
of pyorrhea alveolaris. In the early stages of the disease the probe 
usually fails to discover uncovered alveolar bone, although it may do 
so. If not uncovered its loss is due to resorption; if, however, 
necrotic and bare alveolar bone be found, it is undergoing a molecular 
necrosis under the influence of the pyogenic organisms. 



Fig. 655 



Fig. 656 





Pyorrhea pockets. Mesial root of 
molar largely denuded. Treated by 
amputation. (Price.) 



Section of an upper incisor, showing at 
a, a, a deposit of serumal calculus within 
the free margin of the gum. (Black.) 



In some cases the pericementum may be destroyed at the cervical 
third of the root, the aveolar process may be resorbed on its inner 
surface, and an accompanying constructive irritation may cause 
the deposition of bone upon the outer aspect of the alveolar process; 
the gum margin is also thickened by cell proliferation. The con- 
dition imparts the appearance of hypertrophy of the gum and gum 
margin (Fig. 657). The inflammation of the pericementum may 
become general and the attendant, swelling forces the tooth into 
malocclusion with its antagonist. The mechanical factor is now 
introduced and the extrusion increases gradually or even rapidly. 
Sometimes such teeth can be ground one-eighth inch before removing 
the excess occlusion. Such constant pounding is deadly. 

When about one-half or more of the root has been stripped of 
pericementum and deprived of alveolar support, looseness and 
extrusion of the tooth become marked. 

The advance of the disease now T becomes more rapid; the undue 
mobility and malocclusion of the tooth excite an inflammatory 
reaction beyond the directly infected part; so that soreness and 
looseness are further increased. Extraction at the later stages 
reveals a thickened apical pericementum as the sole attachment to 



720 PYORRHEA ALVEOLARIS 

the bone. After the looseness of the tooth becomes marked, the 
pulp of the tooth undergoes hyperemic changes, reacts to thermal 
stimuli, and is often killed by strangulation of its vacuolar supply. 
Pulp nodules often are formed before its death. Reflex symptoms 
may occur at this stage when the pus pocket approaches the apex. 
(See Pulpitis.) Infection of the dead or practically dead pulp 
readily occurs via the pocket (see Fig. 653), and septic apical perice- 
mentitis arises. The symptoms of the latter condition are modified, 
according to the facility with which the pus finds vent along the 
pyorrhea pocket. In some cases pericemental abscess becomes 
associated. The disease proceeds until the affected tooth or teeth 
are cast out, the alveolar walls having been largely absorbed, and 

Fig. 658 





Section of an upper incisor, showing Section of an upper molar with its 

destruction of the peridental membrane alveolus, etc., showing deposit of serumal 

and eversion of the alveolar wall, with calculus under the gingival borders: a, a, 

thickening of its border: a, serumal cal- serumal calculus. (Black.) 
cuius; b, thickened border of the alveolar 
wall; c, pus cavity. (Black.) 

the pericementum largely destroyed. The remainder of it is usually 
swollen. The disease ceases with the loss of the affected teeth, 
leaving a flattened or absent alveolar ridge covered by a mass of 
more or less spongy gum tissue. 

The duration of this disease may be months or years, and a number 
of teeth may be affected at once. A general subcatarrhal condition 
of the mouth usually attends the disease. The presence of pus 
often imparts to the breath a peculiar, sweetishly fetid odor which 
may, however, be masked by an odor of putrefaction (pigstye or 
sewer-gas odor). 

It is often the case that the shifting of pyorrhetic teeth permits 
the other teeth to move into a position in which they malocclude. 
This brings in a mechanical cause of interstitial gingivitis, which, 



PYORRHEA ALVEOLARI& AS A MARGINAL GINGIVITIS 721 

with the existing infection, brings other teeth into the pyorrhetic 
state. 

Associated Abscess. — In a number of cases of deep pyorrhea pockets 
an infection of the areolar structure, or, at least, of the tissue remain- 
ing over the deepest portion of the pocket, may occur, and an abscess 
form which discharges by a fistula through the labial or lingual 
aspect of the gum. It is to be regarded as an abscess secondary 
to a primary pyorrhea alveolaris. The passage of a silver probe 
through the two sinuses at once will reveal this (Fig. 660). In a 

Fig. 659 




Inflammation of pericementum, endarteritis obliterans. Talbot's case. (Latham.) 



tooth treated for apical abscess such a pyorrhea pocket existed, and 
doubt arose as to the cause. The fact that it was near the gum 
margin and the probe could not be passed into a sinus leading to a 
root-end was considered evidence of abscess secondary to pyorrhea. 
Evacuation and antisepsis were sufficient to effect a cure. 

•In one case of pyorrhea alevolaris of the variety under considera- 
tion the pocket existed upon the mesobuccal aspect of a right lower 
third molar. The second and first molars were absent. The pus 
dissected away the periosteum of the bone and formed a large abscess 

4a 



722 



PYORRHEA ALVEOLARIS 



over the entire area of bone between the third molar and second 
bicuspid. After evacuation of the abscess, the probe was passed 
through it to the pyorrhea pocket (Fig. 661). Another expression 
occasionally occurs. The infection travels via the natural channels 
in the pericementum from the pyorrhea pocket to a deeper point 
in the pericementum (for example, to a point one-quarter inch or 
more below) producing what is called a pericemental abscess. The 
tissue between may seem unbroken and the fistula may seem like 
that associated with chronic apical abscess. Fig. 662 will illustrate 
the manner in which this may occur. In a case of a pyorrhea pocket 
on a lower lateral, transillumination showed a bright red spot at 
a point a quarter-inch below the pocket, and to the side of the root. 
The pain was intense, and only relieved by opening at this point 
with a lancet. In another case a fistula appeared on the buccal 



Fig. 660 



Fig. 661 





Gingival abscess secondary to pyorrhea 
alveolaris: C, calculus in pyorrhea pocket; 
F, fistula leading to pocket PP; B, bone 
on lingual side. 



Diagram of abscess secondary to pyor- 
rhea alveolaris (see text) ; PP, pyorrhea 
pocket; AC, cavity of secondary abscess; 
B, bone. 



gum about one-third inch above the margin and between the 
buccal roots of an upper molar. The crown was tapped by a 
student for dead pulp, but exposure of the pulp demonstrated 
its vitality, Exploration showed a distolingual pyorrhea pocket 
leading into the bifurcation between the distobuccal and lingual 
roots. From thence the pericemental abscess discharged buccally 
between the buccal roots. 

While dental caries may occur with pyorrhea alveolaris, it is usual 
to find the teeth of the most highly organized structure. The pulp 
tissue is usually increased in density, and there is a tendency to 
the constructive changes, secondary dentin, nodules, etc., and the 
inevitable degenerative changes following these diseases. 

It has been contended that these pulps are responsible in a measure 
for the pyorrhetic condition, and it is possible that they may, by 
reflex action, influence the tissue nutrition of the pericementum and 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 723 

gum margin, though the contrary process is more than probable, 
as pyorrhea frequently causes a pulp hyperemia which subsides with 
the cure of the pocket. If the pulps be degenerated, which is likely 
in very loose teeth or deep pockets, their removal aids the cure of 
the disease by diverting the blood they receive into the pericemental 
bloodvessels. This probably counterbalances the effects of the end- 
arteritis obliterans. (See Deeply Seated Gingivitis.) 

Fig. 662 




Pericemental abscess associated with a pyorrhea pocket. (V. A. Latham.) 



It is also true that calculus does not seem to form as readily upon 
a devitalized tooth as upon one containing a vital pulp; it does form 
at times, however. 

Diagnosis. — The diagnosis is easily made when the disease is 
established by observance of the phenomena just described. In 
difficult cases with pocket approaching the apex or bifurcation, a 



724 PYORRHEA ALVEOLARIS 

skiagraph may be necessary for accurate determination of the extent 
of the disease (Fig. 655). 

Prophylaxis. — As outlined above, the prevention of pyorrhea 
alveolaris of the first class involves the removal of the local and, if 
possible, the systemic causes of the gingivitis, if any exists, and the 
systematic cleansing of the teeth at short intervals. The daily use 
of the tooth-brush and antiseptic powders and washes by the patient 
is also important. 

D. D. Smith advises, for this class of cases, a thorough cleansing 
once a month, or at first even oftener. The cleansing is to be done 
with an orange- wood point, grasped in a Jack porte-polisher and 
charged with pumice paste, best made with hydrogen dioxid. The 
local sources of gum infection are thus continually removed and the 
gums stimulated by the mechanical irritation with the wood point. 
Bridges require careful cleansing. (See pp. 441 and 737 for further 
ideas of prophylaxis.) 

Treatment. — The treatment of well-established pyorrhea alveolaris 
of the first class is to be considered under three headings: (1) The 
removal of pus, calculus, and bacterial films; (2) the prevention of 
extreme mobility; (3) the medicinal treatment and the prophylaxis, 
or prevention of a relapse into the diseased condition. 

The Removal of the Causes. — Calculus being an obvious irri- 
tant, it should be removed from crowns and all parts of the roots. 
To prevent infection of surrounding tissues and to remove the pus 
present the pockets are to be flushed out with hydrogen dioxid, 
which may be done by means of a syringe with fine nozzle after 
spraying out the superficial parts by means of an atomizer operated 
by compressed air. The forcible spray lifts away the gum margin 
and cleanses mechanically as well as chemically though not the 
depths of the pockets. The mouth is reasonably sterilized at the 
same time. If large quantities of supragingival calculus exist, it 
is well to next remove the gross deposits and permit the patient to 
use an astringent, antiseptic mouth wash for a few days, or the 
operation may be proceeded with. 

Following this, cotton containing 10 per cent, trichloracetic acid 
may be packed into the gum pockets in order to superficially con- 
stringe the gum tissue, lessen the hemorrhage, and render more 
facile the removal of the subgingival calculi. The latter is accom- 
plished with scalers of any suitable form, working either with a 
push or pull cut as best suits the case. 

Fig. 663 illustrates the method of guarding against unnecessarily 
wounding the soft tissues. If the calculi be extraordinarily inacces- 
sible the pockets may be enlarged by packing for ten or fifteen min- 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 72-") 

utes with cotton tampons saturated with the 10 per cent, trichlor- 
acetic acid, which also softens the calculi, or salicylized cotton may 
be left in the pocket for a day. (Black.) In some cases novocain 
injections or applications of powdered cocain carried into the pocket 
on the working instruments must be made to prevent excessive pain. 
After removal of the bulk of calculus with scalers any fine granules 

Fig. 663 




Showing the manner of holding an instrument for detaching calcareous deposits 
when using the pushing motion. The third finger rests on the edges of the teeth, allow- 
ing freedom of the hand to make rapid and effectual movements in dislodging the 
calculi. 



or gummy collections should be well rubbed off with Rhein's approx- 
imal trimmers,, or Smith's pyorrhea instruments. After this medi- 
cinal applications are made (see later) . The scaling of each tooth is 
to be completed at one sitting, though more than one may generally 
be done, as repeated scalings interfere with the regenerative process, 
and the pocket is most accessible at that time. Hartzell claims that 



726 



PYORRHEA ALVEOLARIS 



if the cemental surface be scraped away to the depth of the attach- 
ment of the peridental fibers a source of infection lying in these 
minute openings will be removed, and the surface will be left smooth. 1 
The lacunae of the cementum should not be invaded. 



Fig. 664 



Fig. 665 





Scalers (three times natural size). 



Illustration of the position and form of 
incision through the gum for exposing the 
root of the tooth and injured alveolar pro- 
cess: a, incision. (Black.) 



The gum margins are not to be unnecessarily wounded, but very 
redundant granulations may be cut away. In case the pockets 
are so deep or have such form that the aveolar margins cannot be 
well trimmed without overstretching or injuring the gingival edges, 
Black advises that gum flaps be raised, exposing the alveolar margins 
(Fig. 665). A semicircular incision is made and turned back, and 
bleeding checked. By means of sharp chisels the alveolar borders 
are freely scraped, the pockets are flushed with hydrogen dioxid, 
and the flap secured by a couple of stitches. Local anesthesia 
should precede this operation. The same writer advises, in cases 
where eversion of the alveolar margin has occurred, that the process 
be exposed by cuts and broken down by three cuts made with a 
sharp chisel and mallet; the loosened segment of bone to be pressed 
firmly against the root. It is desired next that the entire pocket 
will fill with granulation tissue, and organization of the granulations 
take place, furnishing reattachment. That this occurs in some cases 
is undoubted. A reproduction of alveolar margins also occurs in 
some cases. The hope of good results lies in keeping the parts 
aseptic after all foreign deposits and dead material have been removed. 

In cases of excessive loss of the pericementum of one root it is well 
to devitalize the pulp, as, in all probability, that organ will have 
been overstimulated and will be in a degenerative condition, and 
sometimes is actually infected. An abnormal response to thermal 



1 Dental Cosmos, 1908. 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 727 

changes (ordinary cold) may occur (hyperemia or inflammation), or 
the pulp may fail to respond to extraordinary cold (ethyl chlorid), 
indicating degeneration. If the condition be marked and persistent 
after pocket treatment the pulp should be removed and it is well 
to resort to its removal at once when the pocket approaches the 
apex of the root, as the pulp is apt to be hopelessly affected. It has 
been claimed by Rhein, Smith, and others that the nutrition received 
by it will be diverted into the pericementum, to the benefit of the 
latter. Clinical experience seems to confirm this statement. The 
method also permits the use of pins placed in the root canal as part 
of an appliance fixing the teeth in position. An exposed pocket 
in the bifurcation may be treated by scraping and flowing oxyphos- 
phate of copper cement into it (Figs. 666 and 667). In case of 
hopeless involvement of one root of a multirooted tooth the root 

Fig. 666 Fig. 667 





Pyorrhea pocket in bifurcation. The same treated by scraping and filling 

with gutta-percha or oxyphosphate of cop- 
per. (Radiographs by Price.) 

may be amputated if the remaining roots will endure the strain 
put upon them. Indeed, the other roots are apt to be firmer if 
the adjoining inflammation is thus removed. The canals of the 
roots must have been previously carefully filled. 

Rhein 1 calls attention to the fact that collections are apt to occur 
about the surface left by the amputation, and that postextraction 
resorption of the alveolar process occurs. To obviate this he suggests 
the use of a porcelain root to replace the lost root, and about which 
the tissues contract firmly and remain in a healthy condition. This 
operation Rhein terms " heteroplasty following the amputation of 
natural roots." 

Briefly outlined the process is as follows: 

1. Prepare and fill the root canals as far as the pulp chamber; fill 
this with temporary stopping. 

1 Dental Cosmos, September, 1900, and September, 1902 



728 



PYORRHEA ALVEOLARIS 



2. Amputate the necrosed root by means of a fissure drill, and 
remove. 

3. Coat the root with a film of paraffin to allow for shrinkage of 
the porcelain. 

4. Take an impression of one-half of the root (longitudinally) by 
embedding in plaster; make articulating grooves and pour plaster 
for an impression of the other half; separate and remove the root 
from the plaster. 

5. Burnish matrix platinum into each half of the impression, 
stiffen with porcelain, and reburnish. Complete one side with 
porcelain as in inlay work; in the other fuse a platinum box formed 
over a square platinum pin (this pin should be left in the box until 
the packing of the porcelain about the box is complete). 

6. Flatten the proximating sides of the halves; paint with thin, 
fresh body; press together and fuse. 

7. Strip off all platinum and dress off all protruding points, coat 
the entire porcelain with a thin film of body, place in furnace in an 
upright position, and heat almost but not quite to a glaze. 

Fig. 668 




Heteroplasty following the amputation of natural roots. (Rhein.) 



8. Wash out socket of natural root with antiseptics and remove 
temporary stopping from the crown cavity; try porcelain root in 
place, and if right dry everything; fill the box with cement, return 
the root to place, and pass the pin through crown cavity and into the 
root box. Adjust root, leaving a slight space for an amalgam joint. 

9. Pack the crown cavity and the joint with amalgam, and at a 
later sitting finish the same (Fig. 668). 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 729 

The Prevention of Excessive Motion. — The excessive move- 
ment of loosened teeth but increases the deeply seated gingivitis in 
the remaining tissues. These demand rest. Any excessive occlusion 
due to the swelling of pericemental tissue may be compensated for 
by grinding the occluding surfaces. Such excessive occlusion and 
motion are readily detected during the act of occluding the teeth 
or by means of carbon paper. The fixation of teeth is a matter of 
mechanics, and the device used depends upon the case. Slightly 
loosened teeth may be temporarily splinted with ligatures of wire 
or floss silk. To prevent the slipping of these toward the gum 
margin it has been suggested 1 that small buttons of Harvard or 
other adhesive zinc phosphate should be placed upon the labial faces 
while under the rubber dam (Fig. 669). The floss silk may be 
saturated with a solution of chemically pure celluloid in acetone 

Fig. 669 Fig. 670 






Temporary splint of silk floss or silver wire 30-gauge (one turn only shown) . Buttons 
of zinc phosphate. (Rhein.) 

(155 to 500 gr. 2 ) to render it impermeable and more lasting. The 
preparation after application is allowed to dry under the dam to a 
coagulum and then dismissed for twenty-four hours, when it may be 
polished. It lasts for several months. The wire should ordinarily 
be of brass, as it is less likely to permit caries, and may be applied 
as a single strand being woven in figure-of-eight fashion, or a single 
loop may be made about all the teeth to be included and smaller 
loops about the wire at the interspaces, and these twisted tight to 
effect a tightness of the first wire. The fault in ligatures is that some 
mobility is always present. They may slip toward the gum, in which 
case a loop or two may be carried over the occluso-interproximal 
embrasure. For certain cases Dr. Hugh Mitchell has suggested a 
bar of iridioplatinum wire adapted to the lingual surface of the 
teeth to be splinted, and soldered to simple gold bands to be attached 

1 Reitz. 2 Kowarska's paste. 



730 



PYORRHEA ALVEOLARIS 



with cement to two of the teeth adjoining the loose teeth. The 
other teeth are braced to the splint with fine wire; gold or platinum 
being preferred for anterior teeth. 



Fig. 671 



Fig. 672 





Diagram showing labial view of Mitchell's 
splint, with two bands and wiring. 



Diagram showing view of Mitchell's 
splint with two bands and bar. 



Such a splint may be quickly made and is very effective, all slipping 
of ligatures being prevented; moreover, the wire may be kept away 



Fig. 673 



Fig. 674 



Fig. 675 






Five rings and included artifi- Two rings and included artifi- Method of making 
cial tooth. (Evans.) cial tooth. (Evans.) rings as in Fig. 538. 

from the necks of the teeth and the gums. (Figs. 671 and 672.) 
After a reasonable period of immobility the attachment secured 



Fig. 676 



Fig. 677 





Labial view of a splint (see text). Lingual view of splint shown in Fig. 676. 

Fig. 678 



crrrro 

Occlusal view of the splint. 

by treatment may be tested. Very loose teeth which have lost 
much of their supporting alveolar process must be secured by per- 
manent splints. The simplest of these is a series of rings soldered 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 731 

together, or its equivalent, shown in Fig. G70. The teeth are firmly 
ligated at their necks with floss silk. A wire measure is taken of 
the entire circumference of the teeth to be included, allowance being 
duly made for burnishing. A piece of thin platinum or 22 k. gold, 
No. 34 gauge and one-eighth inch wide, is cut to measure and a lap 
joint made and soldered. The ring is placed upon the teeth and 
moulded to their surfaces and to their interspaces. The thinnest 
separating saw is used to cut almost through the splint on both 
sides at one interspace. In this groove a straight piece of the plate 
is placed and the whole withdrawn from the teeth and the joints 
soldered. The process is repeated at another interspace and so on 
until the piece is complete. If the teeth are very tender, a plaster 
impression of the tips of the teeth may be taken and the work done 
on a fusible metal model. If space be necessary, the teeth may be 
slightly disked upon their proximal sides. If such spacing be not 
desirable, the necessary room can usually be obtained at the median 
interspace, but one platinum septum is placed and the piece is to be 
somewhat stiffened with solder at the indentations representing the 
interspaces. To render the appliance less conspicuous the entire 
lingual side may be stiffened with solder and solder be placed liber- 
ally at the junction of band and septum on the labial side. Nearly 
all the labial portions of the bands except the end ones may be cut 
away, leaving T-buttons at the labial portions of the septa (Figs. 
676 and 678). The teeth may loosen in this more readily than in 
that shown in Fig. 670. 

Another valuable device consists in grinding steps into the lingual 
surface of an incisor or cuspid. Soft thin metal is adapted. Three 
pins, No. 20 guage, are placed, two incisal straddling the pulp and 
one at the cervical step. The whole is stiffened with- solder. Adjoin- 
ing teeth may be united by union of these plates or they may be 
used as anterior abutments of bridges. 

It may also be used on centrals and cuspids. For FlG - 679 
example, in a case of loss of an upper cuspid and 
lateral the two centrals were fitted with the tripod step 
plates in Fig. 679 and the first bicuspid with a Carmi- 
chael, the pontic teeth then attached. No pulps were 
devitalized. In bicuspids the Carmichael attachment forms a very 
strong abutment. 

Evans' method is readily comprehended by reference to Figs. 
673, 674, and 675. 

'These splints are to be cemented with adhesive zinc phosphate so 
manipulated as to set quickly. Ames' cements are excellent. 

The foregoing splints are too conspicuous for use in some cases 



732 PYORRHEA ALVEOLARIS 

A simple device introduced by Dr. L. C. Bryan 1 consists of a pure 
gold band about one-eighth inch wide, nicely bevelled at its edges, 
and adapted about the necks of the lower incisor teeth to be splinted 
in somewhat the same manner that the splint illustrated in Fig. 670 
is adapted. Particular attention is paid to the interspaces in the 
endeavor to bring the labial- and lingual sections together as nearly 
as possible at that point. When ready the piece is sprung off, the 
rubber dam is applied, zinc phosphate is placed within the band and 
upon the necks of the teeth at all points, and the band is put in 
place and burnished. Before the cement has set gold wire is to be 
passed around the interdental portions, tightly twisted, and the 
twisted end cut off nearly to the band, and the remainder bent back 
into the indentation in the band. Dr. Bryan recommended gold 
clamps in the place of wire, but these are difficult of adaptation. 

Such a piece is to be placed only on those lower incisors about 
which salivary calculus promptly collects, and should be avoided 
in the mouths of patients who will not present frequently for pro- 
phylactic service. Confined to such cases they do good service, and 
the cement does not readily wash away; indeed, a slight coating of 
calculus seems to protect the surface of it from solution. If the 
calculus be kept from the gum this remnant does no harm. 

Several devices have been offered which require the devitalization 
of the pulps and filling of the root canals of the several teeth to be 
splinted. 

D. D. Smith 2 suggests reduction of the lingual surfaces of the 
teeth and the fitting to them of thin metal backings, which, after 
adaptation to the teeth, are perforated and pins are thrust through 
for the root canals. After soldering each pin to its plate, readapting 
the latter and stiffening with solder, an impression is taken and the 
plates are united. The whole piece is cemented to place with oxy- 
phosphate. A modification for vital teeth would be to drill three 
safe pits for pins for each plate instead of the one central pin for 
the canal, or to drill one hole through the incisal portion above the 
pulp for each plate. With this device one or more artificial teeth 
may be included to replace lost teeth (Figs. 680 to 684). The 
incisal edges, if broad, could have individual inlays cast on two 
safely placed pins (Fig. 277) and these soldered together. 

Ames 3 suggests that in certain cases of lower incisors the teeth be 
devitalized and amputation be performed at the neck of each. Each 
root is then trimmed and fitted with a gold Richmond cap without 
pin (Fig. 683). 

1 International Dental Journal, 1899. 

2 Dental Digest, 1902. 3 Dental Cosmos, 1903. 



Fig. 680 




Splint for securing previously treated lower 
anterior teeth. (Ames, after Smith.) 

Fig. 682 




Splint for use in the case shown in Fig. 681. 
Fig. 684 




Same as Fig. 681. Splint in position. 
Fig. 685 






Upper teeth prepared for splint. 
(Ames.) 

Fig. 683 




Root with cap fitted. (Ames.) 
Fig. 686 




Tooth with Richmond cap. (Ames.) Splint for lower incisors. (See text.) (Ames.) 



734 PYORRHEA ALVEOLARIS 

Each natural crown is slightly trimmed and fitted with a gold 
Richmond cap with a pin (Fig. 685). These two caps are united 
with wax, carried to the mouth, and adjusted in position. Each is 
then carefully removed, the natural crown laid aside (in water), 
and the gold sections invested and soldered together. The individual 
parts are readjusted in the mouth, an impression taken, an invest- 

Fig. 687 




Splint for lower incisors. (See text.) (Ames.) 
Fig. 688 




Splint and double saddle bridge combined. Front view. (Ames.) 

ment made, and all soldered together. The natural crowns are then 
fastened in their prepared sockets with cement, and the piece is 
cemented to place. Pins may be placed in the roots if desired 
(Fig. 686). 

If desired the piece may be further attached to the adjoining 
teeth by means of the lingual plate and pin (Fig. 687). The Ames 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 735 

device would be useful in eases in which approximal cervical caries 
exists. 

It may be stated that three or four teeth fairly loose individually, 
when united together may, as a whole, be quite firm. 

Ames claims that the extension bridge shown in Figs. 688, 689, 
and 690 lasted for years and was in as good condition then as at the 
beginning. Fig. 688 gives the anterior view, Fig. 689 that of the 
right side, and Fig. 690 that of the left side. 



Fig. 689 



Fig. 690 




Right side of extension bridge shown in 
Fig. 688. 



Left side of extension bridge shown in 
Fig. 688. 



Rhein offers the following: After pulp removal and root filling a 
transverse groove is cut in the lingual side of the central or loose 
teeth and a half-groove upon the mesiolingual aspect of the pier 
teeth. A staple is formed of triangular iridioplatinum wire to fit 
into the root canals of the pier teeth. To this is soldered a pin for 
each of the central teeth. The face of the wire should approximately 
fit the bottom of the groove (Fig. 691). Rhein suggests the following 
method of attachment: (1) Fill the root with a paper point, place 
cement over that, and fill the cervical margin of the cavity and its 
floor with gold; (2) drill through the gold to the paper point, remove 
it, and refit the retaining appliance; when ready set with zinc phos- 
phate, avoiding excess; (3) when this is set cut away to the gold 
and complete the gold fillings. 

A less elegant but still practical method would be to cover the 
pins with' a good, color-keeping amalgam pressed into the excess of 
cement before it has set. The margins are then to be freed of cement 
and the operation completed with amalgam, which later should be 
polished. In undecayed teeth this has no advantage over the method 
shown in Fig. 680; nor in decayed teeth over that in Fig. 685. 



736 PYORRHEA ALVEOLARIS 

Smith's, Rhein's, and Ames' devices permit the use of an artificial 
tooth if necessary. The same may be said for the device which 
consists of a series of gold rings (Evans') . 

For the molars and bicuspids Rhein's device is transferred to the 
occlusal surface (Fig. 692). 

Short metal caps made for the incisal tips of lower incisor teeth 
adjoining a space will successfully hold a bridge tooth. The device 
is, however, rather conspicuous. Well anchored gold inlays joined 
by solder or cast together, or a staple in two or more roots of 
different teeth about which staple fillings are later built may be 
useful. Carmichael attachments will serve for some teeth. 

For the molar and bicuspid teeth it seems good practice to adapt 
short crowns to the teeth trimmed only to the fullest point of con- 
tour, and unite these with solder. Occasionally the bands may be 
slit occlusally and adapted closely without covering the cusps. A 
sort of bridge is thus made which causes the teeth to be firm even 
if all are originally loose (Fig. 693). It is mainly this factor which 
renders bridge-work useful in pyorrhea alveolaris upon isolated 
teeth. If the necks of such teeth are hypersensitive, silver nitrate may 
be used. This device is especially useful when teeth are inclined. 
As an example, an upper third and second molar were fitted with 
short crowns, a first bicuspid with a Carmichael and a pontic 
bicuspid used. The united held the three loose teeth very firmly. 

The use of united barrel crowns reaching the gum margins is at 
times useful, but the configuration of exposed roots may render this 
impossible in some cases. 

By the use of pure gold crowns, which may be stiffened occlusally 
with solder to gain strength, better adaptation at cervical portions 
may be obtained by hand burnishing after cementation of the piece. 

All appliances cemented to the teeth and having a free margin are 
subject in some degree to a solution of the cement. These cases 
should be seen frequently in any event for prophylactic purposes, 
when the condition of the appliance may be noted. 

Extraction and bridge-work may be at once resorted to in some 
of the aggravated cases, though if the appliance be mechanically 
constructed teeth which may be extracted with the fingers may be 
firmly held in splints for years. While this is a fact, good judgment 
may demand the early removal of such teeth before an appliance is 
constructed. 

E. Ewing Roach 1 has suggested that in case of loose incisors drill 
holes may be made from mesial to distal or the reverse, and a plati- 

1 Dental Cosmos, 1908, p. 65. 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 737 



num wire, IS or 20 gauge, be cemented through the several teeth. 
The cases must, of course, be selected. 

If desired the bridge may be made so as to mount the natural teeth 
after their extraction, by constructing sockets of gold for the recep- 



Fig. 691 



Fig. 693 




>> 



Permanent splint for cases of pyorrhea alveo- 
laris in upper or lower incisors. (Rhein.) 

Fig. 692 





Permanent splint for cases of pyorrhea alveo- 
laris on molars and bicuspids. 



tion of the necks of the teeth 
somewhat after the manner 
employed in the Ames method. 
The sockets are then soldered 
to each other and to the 
bridge piers, after which the 
teeth are attached. 

These sockets are to be 
made deep at first, and it is 
well to attach the teeth with gutta-percha in order that the row of 
sockets or a new row may be lowered to fit the gum if desirable. This 
will require the raising of the teeth to the occlusal level. Occasionally 
the use of the overarch bar is demanded to prevent the overuse of the 
teeth acting as piers for bridge-work. The lateral support of teeth by 
plates is occasionally of use in pyorrhea, but the question requires 
careful consideration. (See p. 664.) The prevention of mobility in 
advanced cases may be at times an impossibility. In such cases 
extraction, and the use of artificial teeth, is probably better judg- 
ment than the retention of the teeth until extracted one by one. In 
all cases the element of overuse must be considered and anything 
possible done to prevent it. (Read carefully page 661.) Also 
anything that may induce gingivitis as a riding plate festoon must, 
if possible, be avoided. 

The Medicinal Treatment and Prophylaxis. — Simple cases often 
heal spontaneously after thorough work and antisepsis. If aseptic 
a clot drawn after the irrigation of the pocket with hydrogen dioxid 
is often useful. Some operators depend upon blood flow. In order 
to control the patient and watch the case, any pocket existing after 
a week should be washed out with hydrogen dioxid and then filled 
with balsam of Peru which can be kept ready at hand in a Safety 
Sub. Q syringe. This substance is a mild antiseptic stimulant of a 
47 



738 PYORRHEA ALVEOLARIS 

viscidity sufficient to fill the pockets even though wet, if the needle 
is inserted to the bottom. Thereafter it should be used twice a week. 

If the case refuse to heal there may be calculus overlooked upon 
the roots. An acid is used to soften this if not removable by instru- 
ments. Head recommends the use in the pockets on each fourth 
day of ammonium bifluorid 1 as a solvent of calculus and tissue 
stimulant. It does not dissolve enamel or cementum. The tissues 
are to be protected against burns from any overflow, which must be 
removed. It produces no harm within two minutes. It is to be 
injected with a rubber syringe with a platinum point (Dunn syringe). 

Lactic acid full strength (Younger), trichloracetic acid, 25 per 
cent, strength (Kirk) ; sulphuric acid, 25 per cent, strength (Truman) 
are all solvent for tartar, and stimulant germicides if infection con- 
tinues the ulceration. 

As an astringent antiseptic zinc chlorid deliquesced, or sulpho- 
carbolate of zinc in 10 per cent, solution, or zinc iodid in 10 per cent, 
solution, or copper sulphate, 10 per cent., are all useful. 

As an astringent lotion, zinc chlorid, gr. x to each fluidounce of 
aquae rosae, aquae gaultheriae, aquae menthi piperitae, etc., may be 
applied by the patient daily on a cotton swab made by rolling cotton 
on the end of a tooth pick. It may be diluted to an agreeable astring- 
ence for a mouth wash (or two-minute bath), or tincture of iodin 
may be applied every other day, or iodoglycerol (see p. 680) may 
be painted upon the gums. 

Gentle massage of the gums by means of the finger-tips stimulates 
the tissues and squeezes out secretions. If common table salt be 
used in conjunction the stimulant antiseptic effect is obtained. 
Powdered sulphur is recommended by Gordon White instead. 

The use of a strong stream of water from a syringe is recommended 
by Black to wash away the agglutinin collected. 

Dr. A. B. Harrower has suggested the following formula for a 
powder which has in his own and my hands given good results as an 
astringent antiseptic: 

1$ — Magnesium carbonate lb. j 

Cream of tartar : . . . lb. iss 

Red cinchona bark gij 

Calcined alum gj 

Oil peppermint f3v 

Oil cinnamon . . f giij 

Oil rose geranium f 5J 

All ingredients to be finely powdered. The oils are to be added to the magnesium 
before thorough mixing of the powders. The whole is to be sifted through silk. 

Saccharin may be added to the above as a sweetening agent. The powder when 
wet is almost neutral, and should do no harm in its limited use as a therapeutic agent. 

1 "Tartar Solvent," or "Tartasol," is made by neutralizing hydrofluoric acid with 
ammonium carbonate, filtering, evaporating to half the bulk, adding again an e qual 
bulk of hydrofluoric acid, and again evaporating to one-half bulk (at 90° to 105° F.). 
(Items of Interest, 1909, p. 175.) 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 739 

Black has recommended the use of the 1-2-3 mixture, or phenol- 
camphor, to be put into the pockets every three days, and a few 
drops to be used on the tooth brush. 

1$ — Oil of cinnamon 1 part 

Carbolic acid . 2 parts 

Oil of gaultheria 3 parts 

1^ — Gum camphor, 

Crystal carbolic acid . aa q.s. 

Mix in a mortar to an oily fluid. 

Barrett injects as an amebacide a one-half of 1 per cent, solution 
of emetin hydrochloric! in normal saline solution into the tissue at 
the bottom of a pocket and fills the pocket with the solution, repeat- 
ing this on several consecutive days (see p. 714). 

Regeneration in the pockets should not be disturbed, so that 
unless the pus flow be active one should wait until sufficient time has 
been afforded (about a week or ten days) for granulations to form. 
If pus be then detected the pocket should be again treated thoroughly. 
Good results are obtained from the use of an astringent antiseptic 
wash used in forcible spray from an atomizer or introduced by means 
of a syringe. This should be done daily by the patient. Stagnant 
fluids in the pockets are washed out and replaced by the antiseptic, 
thus inhibiting the bacterial growth in the pockets and the mouth. 

The teeth should be cleansed after meals to prevent media for 
infection lodging about the interstices, after which the antiseptic 
spray will aid in inhibiting bacteria. If the case still refuse to heal 
Beck's bismuth paste may be used. 

]$ — Bismuth subnitrate .30 parts 

White wax 5 parts 

Paraffin 5 parts 

Vaselin 60 parts 

Mix while boiling. 

It is injected from a syringe kept for the purpose. 

Good results from the application of the arrays and high-frequency 
currents have been claimed by Parker, 1 Price, Guy, Satterlee, Tousey, 
and others . 

Raper claims that the otherwise incurable cases are not benefited. 

The local treatment outlined must first be given and the x-rays 
and high-frequency currents used as an adjunct. 

Tousey recommends an x-ray tube made of lead glass except for 
a single window of ordinary glass, through which the rays pass in 
one direction only, and thus both patient and operator are protected 
from the unintentional action of the rays. 

1 Dental Cosmos, December, 1903. 



740 PYORRHEA ALVEOLARIS 

Applications of a minute or two have beneficial effect. The high- 
frequency currents are applied by small vacuum tubes or electrodes 
directly to the gums. They contain and emit violet and ultra-violet 
rays, which not only stimulate the part through the electricity, but 
also produce ozone upon the gum surface and carry it in and also 
produce ozone in the tissue by electrolysis. 

The use of vaccines seems indicated in the more serious cases 
not yielding to local treatment, the predominant bacteria being 
employed in the autogenous vaccines. In past treatments these 
vaccines have only aided in resistance to the pyogenic infections, 
and some report good results from their use. A. H. Merritt 1 claims 
that after exhaustive trial he has found them of no greater use than 
local treatment. As yet no one knows the exact cause of pyorrhea, 
so it can not be said that the treatment has proceeded upon scien- 
tific lines. 

McGehee 2 claims about 50 per cent, of cases improved markedly 
through the use of the Van Cott stock vaccines, of which each bulb 
contains in 1.0 c.c. : Streptococcus, 50,000,000; bacilli coli communis, 
100,000,000; pneumococcus, 100,000,000; staphylococcus (combined 
aureus, albus, and citreus), 500,000,000, killed and in sterile solution. 

He claimed his best results were obtained by beginning with one- 
fourth of the bulb content, 0.25 c.c, injecting at four-day intervals, 
later increasing to 0.50 c.c, and up to six, seven, or eight injections 
all told. An effort has been made to utilize the opsonic index in 
the diagnosis of pyorrhea alveolaris and its treatment by means of 
vaccines prepared from the variety of germ found to be the probable 
infection. It may be stated that the effort is to raise the opsonic 
index, or, in other words, the property of the blood serum which 
assists or promotes phagocytosis, so that the infection may be killed 
out. That is, the resistive force of the patient to the particular 
infection is raised. (See p. 63.) 

Good results have been obtained in some cases by extraction and 
replantation, after root preparation and sterilization of the tooth and 
alveolus. The alveolus may have to be deepened. 

If the interstitial gingivitis underlying the case be of systemic 
origin — i. e., due to auto-intoxication from any disease, the alimen- 
tary canal, the pyorrhea itself, or to drug action — these should have 
attention. The systemic disease should, if possible, be cured by 
correct medical attention. Pyorrhea patients are of the hyperacid 
type (Michaels), and treatment should be directed toward elimina- 

1 Remarks before Pennsylvania State Dental Society, 1914. See Dental Cosmos for 
1914. 

2 Dental Cosmos, September, 1912. 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 741 

tion of waste products and the reduction of hyperacidity by the use 
of alkaline remedies. The bowels should be kept active and the skin 
pores open. Brisk exercise in the open air, if not specifically contra- 
indicated by organic disease, is valuable in both directions. Warm 
baths followed by cold douches and vigorous rubbing stimulate the 
skin. Turkish baths followed by massage directed to stimulation 
of the eliminating organs are valuable unless contra-indicated. Free 
drinking of pure water is necessary to the successful elimination of 
the waste products of the body. The water entering the blood 
increases the blood pressure and flushes the tissues and the kidneys, 
dissolving waste products. Water should be freely taken between 
or before meals in order that digestion be not interfered with, and 
if medicated with salts of lithium the alkalinizing effect and solvent 
action of lithium upon urates are obtained. Patients exhibiting an 
aversion to water drinking are more apt to take it when medicated 
than as a physiological necessity. (See also pp. 105 and 689.) 

The prophylaxis of pyorrhea alveolaris is all important, especially 
in the cases in which chronic disease or malnutrition may not be 
readily overcome owing to confirmed habit of life or advanced stage 
of disease. The local conditions existing even after a cure of pyorrhea 
are such as to invite reinfection, and the establishment of microbic 
plaques, which frequent cleansing of the teeth will remove. The 
system of monthly or, if necessary, more frequent prophylaxis 
advocated by D. D. Smith should be practised. Its good results 
are particularly manifest in this class of cases. Also the use of the 
prophylactic stick by the patient twice a week and the careful and 
proper use of floss is very beneficial. The patient performs these 
manipulations with difficulty, and is apt to backslide. (See p. 442.) 

Recurrence of the condition is probable if the oral prophylaxis or 
systemic treatment be neglected. The simpler cases yield quite 
readily; the advanced ones, in which much of the alveolar process 
is lost, and especially when the gums are flabby and admit food to 
the "pockets, tax the patience of operator and patient alike, and are 
apt to end, sooner or later, in loss of the teeth affected. 

This fact, however, should not prevent the retention of these 
teeth by every means at command during the period for which 
they may be made useful. If, however, any tooth prove an incurable 
source of pus formation, or from the first be likely so to do, it should 
be removed, otherwise the remaining teeth, and possibly the patient's 
blood, are continuously infected. The mouth will often be markedly 
benefited at the start if a few bad teeth are removed, and bridge 
work be inserted, to supply their places, thus removing the indi- 
vidual strain and splinting the remaining teeth. 



742 PYORRHEA ALVEOLARIS 



SYSTEMIC EFFECTS OF PYORRHEA ALVEOLARIS. 

It has been abundantly shown by Hunter and others that the pus 
of pyorrhea and other intense oral sepsis is a source of systemic 
infection, producing effects ranging from gastritis to actual septic 
infection. The importance of this fact is not to be lost sight of, and 
patients are to be informed of the dangers of constant pus formation, 
as well as of the presence of other forms of sepsis about the mouth 
and teeth. 

R. D. Watkins, M.D., has examined the blood of pyorrhetic 
patients, and has found a mild condition of septic blood similar to 
but less than found in puerperal fever and advanced carcinoma and 
in other infective conditions. 1 

Goadby 2 reports the cure of a case of profound muscular weakness, 
mental depression, and insomnia after unavailing general medical 
treatment for neurasthenia, as following the extraction of teeth 
affected by pyorrhea. Vanel 3 cites a case of chronic septicemia with 
symptoms of pallor and asthenia, and ecchymotic patches (see p. 
119) on the legs, associated with pus formation about the roots of 
teeth. The symptoms disappeared in a few weeks after the oral 
treatment. 

Hunter and Leith 4 have described cases of subacute and chronic 
catarrh of the stomach and phlegmonous gastritis due to the ordinary 
pyogenic cocci, such as are found in the mouth, and which the gastric 
juice of the stomach of the particular individual at least was not 
competent to kill. Considering the fact that an oral subacute 
catarrhal condition is established in pyorrhea, the local transfer of 
the infection is not surprising. Park 5 believes many cases of appen- 
dicitis to be due to oral infection. 

Kirk adds to this list pernicious anemia, bronchopneumonia, 
malignant endocarditis, pyemic lymphadenitis, etc., as possibilities 
of secondary infection or extension by natural contiguous channels. 

Hartzell 6 claims that three deaths from septic endocarditis were 
traceable to violent pyorrhea. 

Skinner instances a case of intestinal infection, accompanied by 
nervousness and weakness, with confinement to bed for three months, 
as rapidly and steadily improving after the treatment of a pyorrhea 
with profuse suppuration. Rheumatism and even arthritis defor- 

1 Items of Interest, 1904. 2 International Dental Journal, July, 1902. 

3 Dental Cosmos, 1908, p. 192. 

4 Transactions Odontological Society of Great Britain. International Dental Journal, 
1899. 

5 Surgery by American Authors. 6 Dental Cosmos, 1908, p. 240. 



PYORRHEA ALVEOLARIS 743 

mans have been claimed as associated with pyorrhea, the infection 
being absorbed by the lymphatics associated with the teeth. The 
bacteriology of this relation is now being investigated. The organ- 
ism most often offending is the Streptococcus viridans, which may 
be isolated from the blood of the patients suffering from a general 
infection due to a local focus of infection, whether this be in the 
appendix, tonsil, or a dental abscess or pyorrhea pocket. It grows 
upon blood agar with a green color in its colonies. If the same 
bacterins can be isolated from the blood and the focus and the 
condition clear up upon removal of the latter, the relation is 
absolute. (See p. 631 and Index under Bacteria.) 

PYORRHEA ALVEOLARIS NOT DEPENDENT UPON CALCULUS 

FORMATION. 

A form of pyorrhea occurs in which calculus does not seem to be 
the exciting or contributory cause. It seems rather to be due to 
infection localized in soft bacterial collections in localities protected 
from ordinary friction. 

Sometimes no perceptible calculus can be found upon the roots, 
but a soft gummy collection may be noted. The forms of the necks 
of the teeth readily permit bacterial collections and the infection 
causes a bright red marginal gingivitis. A pocket forms and the 
infection becomes deep. The gum tissue is sometimes destroyed 
between two teeth. There is often evidence of infection of other 
gum margins with the bright red color. In another form the gum 
margins are separated from the teeth. Pockets are formed which 
collect food. There is not much pus apparent, but there is a pig- 
stye odor of putrefaction. The marginal bone is lost. In another 
form a deep pocket forms and necrotic bone may be found. 

The advance of the disease is sometimes rapid and sometimes not. 
Sometimes a lateral abscess is associated with it. The diagnosis is 
that of pyorrhea alveolaris of aggravated type, and probably special 
infection, and its progress, symptoms, and treatment are practically 
the same as in the first class. 

The advance of the case may be very slow and limited to the 
teeth originally involved. The following is an example: 

Miss H., aged twenty-five years, presented with well-established 
pockets, extending one-half inch toward the apex, upon the mesial 
aspect of the root of the right upper central incisor and distal and 
distobuccal aspect of the right upper lateral incisor. There was a 
history of traumatism due to violent and persistent wedging with 
rubber at about the age of sixteen. The case was then of several 



744 PYORRHEA ALVEOLARIS 

years' standing, and the two teeth elongated about one-eighth inch 
beyond their fellows (Fig. 694). There was no subgingival calculus. 
The pockets were treated with some benefit, and the teeth shortened 
for the cosmetic effect, but the patient left the city suddenly before 

Fig. 694 




Pyorrhea alveolaris without calculus. Pockets as shown. Teeth were one-sixteenth 
inch longer, but have been shortened. Practically no calculus and but slight flow of 
thick, creamy pus. Gum prominent over affected teeth. Condition in 1904. 

recovery, and was not seen again for three years. At this second 
visit it was found that the pockets were nearly the same as at first, 
and no other teeth had become involved. Nor had the teeth further 
elongated. 

During the four years from 1904 to 1908, elongation and grinding 
reduced nearly all the crown of the lateral, which had one-quarter 
inch of its root cervix exposed. Coincidently with the exfoliation the 
pockets disappeared as though by a drawing up of the bottom. The 
two teeth were finally lost. The consideration of this form of 
pyorrhea should be that it is specially virulent. 



CHAPTER XXV. 

PERICEMENTAL ABSCESS. 

In comparatively rare cases there begins in the lateral aspect of a 
pericementum a swelling which finally discharges its contents either 
at the gum margin or directly through the gum tissue. 

The pulp of the tooth may be perfectly vital and the attachment at 
the gum margin at first at least practically unbroken. A deposit of 
calculus may or may not be formed in the area, and the discharge may 
consist of a glairy fluid or of purulent matter. Cases of this disease 
have been noted and described by Darby (1874), W. E. ^Yalker 
(1895), Talbot 1 (1896), D. D. Smith (1897), and Kirk (1898). Black 
claims that he has never found such a condition without local injury. 

Forms of Pericemental Abscess. — There are four forms of perice- 
mental abscess as described and seen : 

1. x\n ordinary pyorrhea begins at the gum margin and extends 
into the alveolus at the expense of the pericementum. The bacteria 
find their way to the bottom of the pocket or into the tissue at its 
side. They develop in the said location and the pus burrows into 
the lateral gingival tissue, causes swelling and pointing, and dis- 
charges at the lateral gingival aspect or analogous situation. (See 
p. 721.) This is not always opposite the gum orifice of the pocket. 
(See Figs. 660 and 661.) In one case a fistula was found at the buccal 
aspect of the gum opposite a point midway between the buccal roots 
of an upper molar at the middle third of the roots. The pulp was 
exposed and vital, having been drilled to on the supposition of its 
death. A gum pocket was found at the distolingual aspect of the 
lingual root and the pus had burrowed into the bifurcation between 
the lingual and distobuccal root, and discharged as stated, remain- 
ing as a chronic abscess. There is a simple acute condition of this 
kind of origin seen occasionally. A swelling of the gum margin 
occurs and pointing occurs, lancing usually demonstrates pus present 
and effects a cure. The infection has entered the gingival space, 
travelled into the tissue and developed what may be termed a true 
marginal gingival abscess. 

1 International Dental Journal, 1896. 

(745) 



746 PERICEMENTAL ABSCESS 

2. There is a pyorrhetic condition at the gum margin; later an 
abscess develops on the lateral aspect at a point a little higher up 
toward the apex, usually at the gingival third. There may be no 
detectable connection between the two, but probably a deeper 
infection has occurred, the avenue being along the connective tissue 
spaces, the bloodvessels or the glands of Black. In one case of this 
sort the fistula was formed over the highest point of the middle 
third of the root of a cuspid retained for plate work. The gum 
margin was flabby, but not markedly pyorrhetic. There was firm 
tissue at the bottom of the space on all sides. The pulp was vital. 
Examination showed a small calculus on the root surface below the 
fistula. The abscess tract was limited. Sometimes it is of greater 
extent. Fig. 662 will illustrate how this occurs. 

3. An acute swelling occurs over a root, the gum margin is un- 
broken, a discharge of glairy or purulent material occurs, and a 
calculus or none may be found. In this connection Fig. 297 shows 
that a calculus may exist as a primary cause of the pericemental 
abscess. As calculi of gouty (sodium bi-urate) or other origin occur 
in other parts of the body and in the pulp, there is no valid reason 
why one should not occur in the pericementum or upon the root 
under it if some sluggish condition of the circulation renders the 
tissues into a degenerative state favoring it. (See p. 103.) The peri- 
cementum contains white fibrous tissue which is particularly prone 
to such deposits. 

Whether such a deposit occurred primarily in the case of the cuspid 
described under Class 2 and infection followed, or whether the infec- 
tion and pus came first and the calculus followed is not quite clear. 
In two distinct cases, with healthy gum margins, the editor has 
seen an acute circumscribed swelling which was not yet open as a 
fistula and which was perforated by an explorer, disclosing a loss 
of alveolar bone and a small cavity filled with clear liquid in the 
tissues. The explorer reached the root without obstruction, and 
no calculus was present. After discharge and curettement the 
cavities healed. These two swellings looked like blisters or simple 
cystic swellings near the gum margin. If they had discharged at 
the gum margin they might have produced a gum pocket simulating 
pyorrhea. 

4. In some cases of apical abscess the infection may travel along 
the pericementum and develop a secondary abscess at some point 
in the pericementum (as, for example, the bifurcation), as a perice- 
mental abscess. This form corresponds to the cases of Class 2, but 
is apt to be more acute. It is also quite rare. The pulp is, of course, 
dead, at least partially in such a case. 



PERICEMENTAL ABSCESS 747 

The subject of pericemental abscess is in some confusion because 
writers have described all these varying phases as pericemental 
abscess, which indeed they are, yet they require differentiation 
into : 

1. Cases occurring as a sequel to a distinct pyorrhea alveolaris, 
Class 1. 

2. Cases associated with marginal pyorrhea cases but distant to 
them, in all probability having a source of infection in the pyorrhea 
pockets, Class 2. 

3. Cases beginning on their own account; the relation of the cal- 
culus if present as a cause or result being in doubt, Class 3 (Figs. 
658 and 659). 

4. Cases beginning in an apical abscess infection, travelling via 
the pericementum to another portion of the pericementum, Class 4. 

Kirk's studies show that in a few cases of pericemental abscess 
the pneumococcus may be found in pure culture. This suggests a 
Class 2 case, as they are found complicated by other pyogenic bacteria 
in the ordinary pyorrheas. A metastatic blood infection might exist. 

Garrod found crystals of urates in the serum of blisters in gouty 
patients. In gouty patients they are found in joints, and they con- 
stitute the common tophus. (See p. 103.) "Urates of sodium are 
also discharged through the skin in gouty abscesses, either in liquid 
or solid form, and with or without pus." (Musser.) Musser 1 states 
that a number of these abscesses may discharge without impair- 
ment of the general health or even with benefit to the system. - 

Calculi scraped from the roots in pericemental abscesses exhibit 
in a varying degree a response to the murexid test, the test for 
urates. (Pence.) The reaction may be very faint in some cases, 
being overshadowed by the calcium phosphate which makes up the 
bulk of these masses; in others it is pronounced — i. e., urates made 
up a portion of the deposits. 

Black 2 by test found urates in nearly all concretions, salivary and 
serumal, about the teeth. While he claimed that this proved that 
urates have no causal relation to pyorrhea, the findings seem rather 
to point to frequent presence of urates in the salivary and serumal 
excretions, which may really be a cause of irritation even when no 
obvious symptoms of gout are present. 

Miller's demonstration of a calculus upon an unerupted tooth is 
to be recalled. It seems fairly reasonable, therefore, to suppose 
that in rare cases such a calculus may be the result of either gout 
or a local degeneration and act as an exciting cause. (See p. 312.) 

1 Medical Diagnosis. 2 Dental Review, 1894. 



748 



PERICEMENTAL ABSCESS 



Morbid Anatomy. — Aside from the state of the teeth which show 
evidences of a tendency to secondary dentin and nodule formation, 
it has been noted that the abscess is intrapericemental, not sub- 
pericemental. Figs. 697 and 698 show the inflammatory swelling of 
the pericementum ; the central abscess cavity, and the loss by resorp- 
tion of the alveolar process may easily be calculated. The original 
chronic nature of the local irritation in this case is evidenced by the 
presence of hypercementosis. 



Fig. 695 



Fig. 696 





A and C, vital pericementum; B, gouty cal- 
culus; D, a subgingival calculus. 



A t calculus in area of necrosis; 
B, and C, vital pericementum. 



Fig. 697 




Two views of an intrapericemental abscess. Pulp vital. (Kirk.) 



Symptoms. — These have been largely foreshadowed in the dis- 
cussion of the pathology. Upon some vital tooth there appears an 
uneasiness, at first not very painful, followed later by an inflamma- 



PERICEMENTAL ABSCESS 
Fig. 698 



749 




Transverse section through buccal roots and pericemental abscess shown in Fig. 
697, showing intrapericemental abscess cavity with fistulous outlet and nearby areas 
of nodular hypercementosis. (Kirk.) 



Fig. 699 




Pericemental abscess. (Talbot.) (Photograph by Latham.) 



750 PERICEMENTAL ABSCESS 

tory swelling which may produce acute pain and then discharge a 
glairy fluid or purulent matter. There is an absence of the masked 
phlegmonous inflammatory involvement of contiguous tissues com- 
mon in cases of acute apical abscess. The fistula may persist after 
the discharge and the case may first be seen in this condition. If it 
discharges at the gum margin it establishes an ordinary pyorrhea. 

D. D. Smith calls attention to the absence of marked pain upon 
tapping and the production of a feeling of apprehension upon the 
part of the patient during the stages preceding the formation of the 
fistula. In other cases the shifting of the tooth from its position is 
the first noticeable symptom, followed later by the pain, and later 
still by the discovery of a pocket alongside the tooth. 

Diagnosis. — In making the diagnosis the symptoms described are 
to be borne in mind, but the disease may be confounded with several 
diseases having somewhat similar symptoms. An acute apical 
abscess due to gangrenous pulp may be differentiated by obtaining 
evidences of pulp death, previous root-canal treatment, etc. There 
is also much greater pain upon percussion than in pericemental 
abscess. If slowly and painlessly formed it may be still more con- 
fusing, but the pulp is dead. 

Fig. 700 




A, calculus. 

If the apical abscess be in the third stage it may be differentiated, 
if any doubt exist, by incision and subsequent exploration. 

An acute lateral abscess due to a root perforation is more difficult 
of differential diagnosis, but after incision evidences of perforation 
may be sought externally, or the root canal may be opened. In 
these acute conditions the z-rays may render valuable aid. The pulp 
being found alive by any reliable test is evidence that the case is 
either one of pericemental abscess or of acute traumatic perice- 
mentitis. In a few cases of partial gangrene of the pulp the pulp 
may test as vital, yet really the symptoms be due to apical abscess. 



PERICEMENTAL ABSCESS 751 

Acute traumatic pericementitis usually has a history of traumatism 
and presents more pain upon tapping. Any abscess is usually the 
result of infection due to rupture of the pericementum. The other 
forms of pericemental abscess must be differentiated (see p. 745). 

Treatment. — If the pericemental abscess discharge by way of the 
gum margin, infection from the oral cavity occurs and the pocket 
originally formed becomes deeper. The case simulates then a pyor- 
rhea alveolaris beginning at the gum margin. The treatment is then 
conducted accordingly. If the swelling occur upon the gum, at a 
point more or less midway upon the root, it should be opened under 
antiseptic precautions. An injection of cocain solution should be 
made, if necessary, and a semicircular flap raised. The diseased area 
should be explored for calculus and, whether found or not, the 
necrotic tissue should be curetted away. Next, the pocket should 
be syringed out with an antiseptic and filled with balsam of Peru 
or a clot induced. The flap is next laid into place. The mouth 
should be kept in an aseptic condition during the healing of the 
parts. It is well to have the patient keep the sinus open with a 
needle to ensure healing from the bottom rather than ballooning 
by pus, which may cause recurrences. The systemic considerations 
are the same as those described on pp. 714 and 740. 



CHAPTER XXVI. 
REFLEX NEUROSES. 

Reflex neuroses consist of (1) pain produced in parts distant 
to the point at which irritation is produced, while pain may or 
may not be absent at that point (sensory reflexes), or (2) they may 
consist of muscular excitation in parts distant to the cause (motor 
reflexes), or (3) they may consist of nutritive disturbances in the 
distant part, probably a form of motor reflex in which the trophic 
nerves or the vasomotor nerves are reflexly irritated so as to 
produce trophic disturbances. 

The source of irritation may be in the dentinal fibril, in the pulp, 
or in the pericementum, producing sensory or motor or trophic 
reflexes in other parts or the source of irritation may be in some 
other location than about the teeth and produce phenomena about 
the face or teeth. 

Whether of dental origin or not a sensory reflex is called neu- 
ralgia, though the cause of a neuralgia may possibly be a direct 
irritation of a nerve trunk or terminal. 

While all reflex dental disturbances are, as a rule, located in some 
part of the great nerve branch supplying the source of irritation, 
the irritation may be reflected to distant parts; first, of the same 
cranial nerve, and secondly, to other nerves. That is, pain having 
its origin in one of the upper teeth is most likely to be referred to 
a point or points in the distribution of the superior maxillary divi- 
sion of the fifth nerve. Disturbances in or about the lower teeth 
are usually referred to the distribution of the inferior maxillary 
division. In affections of either upper or lower teeth the pain may 
be referred to the ophthalmic division. In all of these cases, but 
most notably in connection with disturbances of the upper teeth, 
the usual symptom of trifacial neuralgia — tenderness of the supra- 
orbital and infra-orbital nerves at their points of emergence upon 
the face, the supra-orbital and infra-orbital foramina — is commonly 
present. 

Cases are extremely rare where the reflex pain is referred to the 
opposite side; so unusual is this occurrence that its mention 
warrants suspicion that other sources of irritation exist upon the 
side referred to. 
(752) 



REFLEX NEURALGIA FROM EXPOSED DENTIN 753 

The extent of acuteness of reflex pain bears no direct relation to 
the apparent extent of the source of irritation. 

As might be surmised from the function of the dental pulp, painful 
reflex dental disorders are more common in connection with diseases 
of the pulp than with those of the pericementum. 

REFLEX NEURALGIA FROM EXPOSED DENTIN. 

The exposure of the dentin to external sources of irritation is 
followed by reactions governed, first, by the degree of sensitivity 
inherent in the protoplasm of the tissue ; and secondly, by the degree 
of hypersensitivity induced in it. Reflex disturbance due to these 
irritations is more common in the class of persons called "neuralgics," 
i. e., in those whose nervous irritability is exalted, a condition which 
may remain even in nervous exhaustion (see p. 110). Like direct 
pulp pains, unless actual pressure be exerted upon the affected 
tissue, there is no localized pain. In the absence of deliberate irri- 
tation, the pain may be referred to any portion of the peripheral 
distribution of the fifth nerve upon the face, but if an acid liquid, 
such as lemon juice or vinegar, or sugars be taken into the mouth, 
pain is excited, which is referred indefinitely to the teeth of one side, 
frequently of one jaw. Reflex pains due to this cause often appear 
when there is but little loss of dentin. 

When carious cavities have proceeded to any depth evidences of 
direct pulp disturbance are obtained through the increased response 
to thermal changes. 

Reflex pains from exposed dentin appear most commonly in con- 
nection with exposures at the neck of the tooth and upon abraded 
areas. Obstinate and persistent neuralgia, positively referred to 
another nerve branch, may apparently owe its origin to so slight a 
cause as exposure at the neck of a tooth of a line of dentin (Fig. 702) . 
The proof of the connection between the two is made clear by a 
disappearance of the neuralgia after the exposed dentin has been 
subjected to the action of powerful caustics (especially silver nitrate), 
destroying the dentinal filaments to some depth. The connection 
between the two may be revealed only by accident; the contact of 
a toothpick, a dental instrument, or the finger-nail may induce a 
paroxysm of pain. In one case, after removal of calculus, the necks 
of the lower incisors became a cause of severe neuralgia, compelling 
the use of silver nitrate. 

•While in some cases the dental origin of reflex pain may be made 
clear by the induction of a painful response in the area of reflection, 
by irritating a tooth pulp, this reaction is not constant. The causal 
48 




Fig. 701. — Plan of the fifth cranial nerve, showing the relationships of the dental 
nerves. (After Flowers.) 




REFLEX NEURALGIAS FROM PULP DISEASES 755 

relation is only certain when the cure of localized dental disease 
is followed by a disappearance of the neuralgia without further 
treatment. This proof should 
be exacted in all cases. FlG - 702 

The most common sources of 
neuralgic attacks about the face 
are diseases of the eyes and teeth. 
In general terms, diseases of the 
eye give rise to reflex pains re- 
ferred to the distribution of the 

. . „ . „„ , Sites of dentin exposure frequently asso- 

farst branch of the faith nerve: dated with reflex pains, 

diseases of the teeth usually cause 

reflex pains in either the superior or inferior maxillary divisions, 
according as the upper or lower teeth are affected. In all painful 
affections of these nerves attention should at once be directed to the 
organs named. 

REFLEX NEURALGIAS FROM PULP DISEASES. 

The disturbances require classification according to the distance 
between their source and their manifestations. 

In the Fifth Pair of Nerves. — Pain referred to a different spot 
or area than its origin is a characteristic of all pulp diseases. The 
extent of its reflection depends, first, upon the patient, as noted in 
connection with the reflex pains from exposed dentin; and secondly, 
upon the variety of pulp disease. In neuralgic patients any variety 
of pulp disease may cause comparatively distant pains. But, as 
Black has pointed out, 1 the general rule is, that the more chronic and 
profound degenerative diseases of the pulp are much more liable to 
give rise to distant reflex pains than are acute pulp diseases. 

The pains of acute hyperemia and of acute inflammation of the 
pulp are usually referred to the region of the tooth affected, or to a 
corresponding nerve trunk. In conditions of venous hyperemia, 
nodular calcifications, chronic inflammation, and, later, pulp degen- 
erations, the pains may be of such character that their dental origin 
is only determined after persistent search. Particularly is this true 
of the growth of pulp nodules. The source of the reflex pains is all 
the more obscure from the fact that in these chronic degenerations 
direct dental symptoms may be entirely absent, and are only elicited 
upon the most searching examination and exhaustive tests. In some 
cases of pulpitis even removal of the pulp by cocain has been fol- 

1 American System of Dentistry, vol. i. 



756 REFLEX NEUROSES 

lowed by a neuralgia due to irritation of the nerve trunk in the pulp 
stump at the apex, so proved by cure through strong sedatives 
applied via the canal. In one case the neuritis lasted several days. 
There is no constancy in the location of the pain due to any of 
these causes; but tenderness of the eyeball upon pressure; iritis or 
conjunctivitis; persistent pain in the temporal and anterior auricular 
regions, particularly in connection with pulp diseases of the lower 
posterior teeth; in the ear itself, a common site of the reflex pain 
excited by chronic pulp inflammation and suppuration of that organ; 
behind the ear, back of the lower border of the mastoid processes, 
tender spots may develop; tenderness to pressure may appear at 
the supra-orbital and infra-orbital or mental foramen, and about the 
chin. In the same class of diseases the pains may frequently radiate 

as far as the shoulder. Many of these 
FlG - 703 cases receive attention from the general 

practitioner, and the painful attacks re- 
curring at irregular intervals are relieved 
by analgesic remedies — phenacetin, acet- 
anilid, exalgin, etc. — and no attention 
paid to a probable dental source of the 
disorder. It should be a routine practice 
to examine the teeth in cases presenting 
pains of the type and in the situations 
described. Acute diseases of the pulp, 
including suppuration, notably abscess 
of the pulp, usually have attention di- 

bpots of tenderness in reflex . . 

neuralgias of dental origin. rected to the teeth through pam induced 

by thermal changes, so that their diag- 
nosis is quickly made. Not so, however, with the chronic degener- 
ative changes, except possibly of pulp nodules; for if the pulp is in 
the late stages of degeneration, it may require repeated applications 
of cold and heat to elicit a response from teeth which do not respond 
by tenderness upon percussion. 

Failing to obtain evidence of pulp disorders, examination should 
be made for exposed and hypersensitive dentin. Then, examination 
of the pericemental reaction of each tooth should be made, and for 
any evidences about the teeth pointing to pericemental disturbance. 
(See later.) 

Lauder Brunton 1 records that, in his own case, temporal neuralgia 
accompanied by tender eyeball was found due to exposed dentin 
upon the posterior cervical surface of a lower third molar (see Fig. 
702) . The same writer 2 announces that " so frequently are headaches 

1 St. Bartholomew's Hosp. Rep., vol, xix. Reprinted in his Disorders of Digestion. 

2 Ibid. 




REFLEX PAINS FROM DISEASES OF THE PERICEMENTUM 757 

dependent upon decayed teeth, that in all cases of headache the 
first thing I do is to carefully examine the teeth;" as should every- 
one else. Upson cites by radiograph a case of severe headaches of 
years standing, cured by extraction of an impacted cuspid. 1 Brunton 
explains the painful reaction upon the accepted hypothesis of the 
pathology of megrim, that it is due to spasmodic contraction of the 
peripheral end of an artery, with dilatation of the proximal portion. 
"Irritation in the tooth is reflected to the cervical sympathetic 
ganglia and causes spasmodic contraction of the arteries through 
irregular stimulation of the vasomotor nerves." 

An abnormal tooth located in the anterior floor of the nasal cavity 
was the cause of headache for years, so proved by cessation of head- 
ache after its surgical removal. 

REFLEX PAINS FROM DISEASES OF THE PERICEMENTUM. 

As a general rule, pericemental pains are located at the affected 
tooth; but in some of the disorders the teeth may not be tender upon 
percussion, and yet excite reflex pains in other parts, the proof of 
the connection being determined by a disappearance of the pain 
upon extraction of the tooth. The roots in such cases usually present 
either an hypertrophy of cementum or show that resorption of a 
portion — it may be a major portion — of the root has occurred. 

In cases of hypercementosis it is assumed that the source of the 
irritation is pressure upon the nerves of the pericementum by the 
hypertrophic growth. Very widespread disorders may arise from 
this source. 

Flagg 2 records many varieties of trifacial neuralgia; pains in remote 
parts of the body; grave functional disorders of the eye and ear; 
and motor disturbances — chorea, epilepsy, and paralysis — having a 
direct demonstrable connection with hypercementosis. Insanity lias 
also been produced. 

He mentions violent attacks of trifacial neuralgia as the most 
common reflex disturbance from this source ; and next, long-continued 
pains in the ear or eye of the affected side. The existence of acute 
disease of these organs is usually diagnosticated by the general 
practitioner. He states that aural and ocular disturbances, both 
functional and painful, are of gradually increasing severity. 

In examining for a dental source of such pains, exposed dentin, 
pulp diseases, and inflammatory affections of the pericementum 
should be first excluded. In examinations by percussion a different 

1 Raper, Items of Interest, August, 1912, p. 575. 

2 Dental Cosmos, 1878. 



758 REFLEX NEUROSES 

response may be obtained from some one tooth than from the others. 
Hypercementosis of a particular tooth may be suspected by finding 
the gum line slightly receded and the tooth attachment unusually 
firm; if, in addition, vague, heavy dental pains have persisted at 
intervals over a long period, the diagnosis is probable. It is only 
certain when tapping upon the tooth brings on a paroxysm of 
neuralgia, and a skiagraph actually exhibits the hypertrophic 
growth. The remedy is extraction. Any root fragment left unex- 
traeted may perpetuate the reflex disorder. The writer has recently 
treated a case of neuralgia due to a lingual root of a left upper first 
bicuspid which was retained in the gum after extraction. The gum 
had healed perfectly over it. It was only discovered by the use of 
the x-rays. 

Painful affections referred to the neighboring region of the affected 
tooth, or diffused through the distribution of the corresponding 
nerve trunk, or to the eye or ear, may accompany the process of 
resorption of the roots of permanent teeth. Gillman 1 records a case 
where facial paralysis disappeared upon extraction of a tooth which 
had long been the seat of disturbance and which, upon extraction, 
revealed resorption of its root. In these obscure cases a skiagraph, 
if taken at once, will be a great aid in the exclusion or diagnosis of 
pericemental and root abnormalities. 

All of the acute or chronic, septic or non-septic, inflammations of 
the pericementum may give rise to reflex pains. The most common 
causes of the reflex pains are found in that stage of pericemental 
irritation which antedates acute septic apical pericementitis. Unless 
an exacerbation of the reflex disorder, or symptoms referable to that 
region, be induced by pressure or percussion on the tooth, a causal 
relationship is only made out by either relieving an existing dental 
disorder (for example, finding and curing an incipient apical abscess 
due to moist gangrene), an a>ray skiagraph, or extracting the teeth. 

Cases of ovarian and uterine neuralgia and sciatica and cases of 
obstinate pains in the knee, toes, and fingers have been traced to 
dental irritation of some one of the varieties named, the proof of 
association being disappearance of the pain with loss of the tooth, 
though this is now not always necessary for a cure. 

IMPACTED TEETH AS A CAUSE OF NEURALGIA. 

Neuralgia of varying degrees of severity is a common accompani- 
ment of impacted teeth. It is most frequently noted in connection 
with eruption of the lower third molars, not only because this tooth 

1 Boston Medical and Surgical Journal, 1867. 



PHANTOM ODONTALGIA 759 

is the one most frequently impacted, but because of the anatomical 
relations of its roots with the inferior dental nerve. 

In the milder forms of impaction, those in which eruption, though 
delayed, is subsequently completed, the pains are commonly local- 
ized and associated with but occasional attacks of rigidity of the 
masseter muscles. If, however, the crown present horizontally or 
nearly so, and its progress is arrested by impaction against the 
posterior wall of the lower molar, or if its progress be arrested by 
permanent imprisonment of the advancing crown between the pos- 
terior surface of the second molar and the base of the coronoid 
process, not only may intense local pains be induced, but severe 
reflex disturbances of both a sensory and motor character may occur. 
In some of these cases root formation is completed, although the 
crown of the tooth does not advance, in which case compression of 
the inferior dental canal and its contents may occur and cause grave 
reflex disturbances. The local irritation about the root, due to root 
growth, may excite continued constructive action by the peri- 
cementum, and the hypertrophic growth in its turn may be the 
source of reflex neuralgias. 

Complete imprisonment of the entire tooth has been found to be 
the exciting cause of facial neuralgias, for the cure of which extensive 
surgical operations have been performed. 

Impacted cuspids and other teeth may excite no other symp- 
toms than reflex neuralgia. The possible connection between an 
impacted tooth and neuralgia is made out after excluding other 
dental causes, when it may be observed that one or more of the 
permanent teeth are absent from the dental arch, at dates long after 
their normal time of eruption. 

A condition equivalent to partial impaction, in which dental irri- 
tation may be the source of reflex neuralgia, is seen when the teeth 
are crowded into arches too small for their accommodation. During 
the period of eruption severe maxillary pains may recur at intervals. 
The diagnosis is by means of the rc-rays. The production of insanity 
as a reflex condition has been discussed on pp. 294 and 762. 

PHANTOM ODONTALGIA. 

This is a form of neuralgia in which symptoms similar to tooth- 
ache appear in the edentulous jaws or in locations from which teeth 
have been extracted. The name was applied by J. Foster Flagg. 
It seems to be due to the compression of nerve-endings by dense 
bone. It may, of course, be a reflex neurosis from some other focus 
of pulp or pericemental or nerve trunk irritation. 



760 REFLEX NEUROSES 

Any history obtainable of a previous local inflammation should 
be obtained, and if the pain is localized in any spot the bony tissue 
may be broken up by operation with a view to removal of such a 
cicatricial inclusion of nerve terminals. At least in troublesome 
cases such a simple operation is admissible. Cryer reports successful 
operations for removal of a bone whorls," the cause of neuralgia 
(see Fig. 704). 

Fig. 704 




The arrow points to a dark, three-sided shadow — a bone "whorl." The X on the 
shadow is caused by a scratch on the negative. (Radiograph by Pancoast, Courtesy 
of H. R. Raper.) 



PARALYSIS OF THE SENSORY TRACTS. 

The operation of extraction and occasionally disease of the pulp 
and pericementum have produced a temporary paralysis of a branch 



MOTOR DISTURBANCES FROM DENTAL DISEASES 761 

of the fifth pair and loss of sensation in the lip or cheek may result. 
So far as observed the cases are of not more than a few months' 
duration and may be ameliorated by massage, either passive or 
vibratory or by faradization. 

MOTOR DISTURBANCES FROM DENTAL DISEASES. 

Motor disturbances due to dental irritation may occur as recurrent 
or persistent contraction or paralysis of muscles, together with more 
or less chorea; in rare instances epilepsy and hystero-epilepsy. 
Twitching of muscles of the affected side of the face, ranging from 
slight affection of the occipitofrontalis or orbicularis palpebrarum 
to recurring spasm of the elevators and depressors of the lower lip, 
are far from uncommon phenomena attendant upon pulp and peri- 
cemental diseases. In one case mentioned by Guilford 1 a pulp 
nodule was the cause of tic douloureux (painful muscluar contrac- 
tions) of two years' standing. Varney Barnes cites a case of " blinking 
of the eyes," caused by an impacted tooth. 2 A case of recurrent 
epileptic attacks was proven due to a tooth brush bristle forced into 
the gum. 3 (See also p. 464.) 

Contraction of the masseter muscle is a common accompaniment 
of retarded eruption of the lower third molar, which may be inten- 
sified until the condition is fitly termed trismus, in some cases of 
partial impaction of the teeth. Partial trismus has been found due 
to a general overcrowding of the dental arch. 4 Records of cases of 
torticollis, due to dental diseases, are also given by Brubaker. 

Cases of facial paralysis, and cases of paralysis of one arm, of 
paraple'gia and hemiplegia, and even of general paralysis, have been 
noted as disappearing after the extraction of diseased teeth. It is 
noteworthy that in these cases, as well as in several cases of tetanus 
recorded, the probability of an infection entered into the patho- 
genesis of the nervous diseases. 

Stellwagen 5 records a case where symptoms of partial hemiplegia 
followed upon the operation of capping the pulps of two molar teeth; 
the symptoms disappeared promptly upon extraction of these teeth. 
A case of facial paralysis followed extraction of seven roots upon one 
side. It was successfully treated by eight applications of a weak 
galvanic current. 6 Facial paralysis has also followed the eruption 
of teeth, as of a second molar. Infantile paralysis has also been 
caused by dentition (see p. 203). 

1 Private communication. 2 Raper, Items of Interest, August, 1912, p. 575. 

3 Dental Cosmos, 1910, p. 594. 

4 Brubaker, American System of Dentistry. 

Private communication. 6 Griefswald: Cosmos, 1906, p. 356. 



762 REFLEX NEUROSES 

Cases of insanity arising from dental diseases have been recorded; 
they were both maniacal and melancholic. In several of them a 
restoration to a normal mental state followed promptly upon removal 
of the offending teeth. In some of these cases a preexisting maxillary 
neuralgia directed attention to the teeth as possible sources of the 
nervous diseases. 

Dr. E. Ballard Lodge 1 reports a case from the practices of Drs. 
Upson and Stephan in which a lady had suffered from acute melan- 
cholia and insomnia. A skiagraph revealed an impacted upper 
third molar pressing against the distal side of the second molar. 
Extraction effected a cure. Upson 2 reports a number of like cases, 
as well as some due to pulp and pericemental disease. The local 
conditions were painless. (See p. 294.) 

Cases of deafness have been recorded due to diseases of both pulp 
and pericementum, notably to hypercementosis. Deafness which 
has persisted for a long period has been markedly lessened by the 
extraction of teeth the seat of disease. Cases of suppurative otitis 
media have been regarded as having pathological association with 
septic diseases about the teeth, from the fact that the aural trouble 
subsided immediately after extraction of the diseased teeth. 

Sensory disturbances of the eye, associated with dental diseases, 
have been alluded to; in addition to these, grave structural and 
functional diseases of the eye, traceable to dental causes, have been 
recorded, such as motor and trophic disorders. 3 Among the latter 
may be mentioned corneal inflammation and ulceration and phlyc- 
tenular conjunctivitis. These are probably due in part to reflex 
trophic disturbances. 

Irregular paralyses of the third, fourth, and sixth nerves of the 
affected side have been noted. 

Amblyopia and functional blindness without retinal conditions 
to account for it have been found to arise from notably advanced 
degenerative changes in the dental pulp, sight returning to the eye 
after loss of a diseased tooth. DeWitt 4 records a most instructive 
case where temporary blindness was associated with septic apical 
pericementitis, disappearing after evacuation of the abscess and 
reappearing when secondary inflammatory action arose in the peri- 
cementum. The ocular affection disappeared permanently and 
almost entirely with the loss of the tooth. The history of this case 
illustrates the important causal relationship of reflex disturbances 

1 Dental Summary, 1908. 2 Dental Cosmos, 1910, p. 526. 

3 See Brubaker, American System of Dentistry, vol. iii, for very full and detailed 
discussion of these subjects. 

4 Quoted by Brunton, Disorders of Digestion. 



DENTAL PAIN FROM OTHER THAN DENTAL SOURCES 763 

with late pulp degenerations; for the blindness arose two months 
after some teeth were filled, and existed for twelve years before the 
septic apical pericementitis appeared. 

Trophic Disturbances following Dental Diseases. — Two cases of 
localized alopecia (loss of hair) have been reported, 1 obstinate during 
the dental disease and cured by the cure of a pulpitis in one case 
and extraction of a root for suppurative pericementitis in the other. 
Such cases show a vasomotor disturbance in the distant part. 

DENTAL PAIN ARISING FROM OTHER THAN DENTAL SOURCES. 

Conditions of pain the reverse of those discussed— i. e., pain 
definitely or indefinitely located in teeth which exhibit no morbid 
conditions whatever — demand occasional attention at the hands of 
the dentist. 

Chronic malarial poisoning, as stated in the beginning of this 
chapter, may give rise to periodical attacks of maxillary neuralgia. 
As in the gouty cases, the constitutional cause of the disturbance is 
made clear through the therapeusis most effective, viz., the periodical 
recurrence of the pain leads to the inference of a malarial origin, and 
to the administration of quinin. Anemia and other conditions in 
which there is accumulation of products of metabolism also cause it. 

Syphilitic pains in the jaws have a pericemental character, and 
other evidences of syphilis are present which point to a diagnosis. 

Pains in or about the teeth are occasional accompaniments of 
diseases of the brain or its vessels, and of pregnancy or diseases of 
the uterus, kidneys, and bladder. 

Disea'se in any portion of the fifth cranial nerve may cause pain 
referred to the teeth, for example, inflammation of the nerve trunk, 
a tumor in the nerve, or a tumor pressing upon the nerve trunk, 
or a portion of fractured bone so pressing, or a cicatrix contracting 
upon a nerve. 

Dental pain during pregnancy, without any direct evidence of 
dental disease, is relatively common. 

Disorders of the lower bowels, causing constipation, may give rise 
to pain referred to one or more teeth, the pain ceasing promptly 
upon the administration of an active evacuant. 

La grippe occasionally produces antral empyema or neuralgia 
about the dental region as one of its sequelae. 

Pain may appear in one or more teeth either with or without 
association with pain about the maxillae or tenderness at the foramina 

1 Mounier: Le Laboratoire, 1907. 



764 REFLEX NEUROSES 

of emergence. If there be possible causes in defective teeth or teeth 
with fillings in which pulp irritation is a possibility, there may be 
difficulty of diagnosis. There may be a history of an attack of 
influenza or even of coryza, with the common variety of which 
dental pains are often associated. Abscess in the maxillary sinus 
or other sinuses may do the same. 

It may occur after la grippe has seemed to have disappeared. The 
pain is at first generalized over the entire head, but gradually local- 
ized in one or several upper teeth, more frequently in the second 
molar, occasionally the bicuspids. It sometimes is so severe that 
the patient thinks an abscess is forming. 

There is almost always pain in the molar region when pressure is 
made upon the inner alveolar portion of the hard palate, and sensi- 
tivity of the external alveolar region. 

For the pseudoodontalgia Roy recommends a capsule containing 
the following: 

1$ — Antipyrin gr. vij 

Quinine hydrobromid . . . . , . . . • . . gr. iij 

Sodium bicarbonate gr. iij 

Sig. — One dose. Increase and prescribe four times a day. 

Locally he recommends: 

1$ — Mentholis gr. x 

Acidi borici 5iij 

Vaselini gj — M. 

Sig. — A small portion to be applied within the nostrils on rising and retiring. 

Treatment of Facial Neuralgia. — The cause. should be sought for, 
and, if possible, removed. If due to disease of the teeth, these should 
be relieved; if due to eye disease, or other cause, this should receive 
attention. Should one not discover the cause, yet desire to afford 
a relief pending its discovery, the accepted remedies antipyrin, 
acetanilid, and phenacetin, combined with caffein or the bromids, 
are useful. 

1$ — Antipyrini (vel phenacetini vel acetanilidi) . . . . 3.1 

Caffeinse citratis gr. x 

Potassi bromidi . 3ii.i — M. 

Ft. in chart No. x. 

Sig. — One every thirty minutes until relieved. (Hare.) 

If the patient be constipated, the bowel should be freed of toxic 
substances by the use of castor oil, repeated as necessary. Castor 
oil in small doses is antineuralgic. 

In obstinate neuralgia and other painful affections with unremov- 
able cause, the application of the arrays has been urged by Morton 
as highly efficacious in relieving pain, often for a considerable time. 



TREATMENT OF FACIAL NEURALGIA 765 

The blue ray is also used. A remedy of exceedingly simple nature 
was introduced by Verge and Pitres in 1902. It consists of injecting 
into the mucous membrane or skin, about where the pain seems to 
originate, 1 c.c. of alcohol (85 per cent, plus 1 per cent, cocain is 
preferred by Lenson) at the temperature of 60° C. by means of a 
hypodermic syringe. Asepsis must be provided for. 

A slight humming sensation and swelling of tissue occurs about the 
area of injection. The pain disappears for a long period after one 
or two injections a week apart. 

Dr. H. I. Patrick 1 recommends the injection in trifacial neuralgia 
not dependent upon recognizable conditions as preferable in the 
middle aged and aged to the Gasserian operation, and sets forth 
the landmarks as well as the conditions for the operation. 

The Gasserian ganglion has also been injected with alcohol with 
apparent satisfaction, and is less serious than radical operation. 

A deep injection into the nerve trunks has high medical indorse- 
ment. A case in which the face became black on the side of injec- 
tion was also followed by relief and subsidence of the congestion. 
The method has been objected to by some. It has been recorded 
that myosis, and prickly or tingling sensation or paralysis of the part 
or nearby muscles of temporary nature are by-effects. Injection 
of the nerve trunk with dilute osmic acid has been practised by 
surgeons. 

Strychnin in fairly large doses has been employed under medical 
supervision. When the cause cannot be determined the nerve itself 
may be resected. These are mainly measures in the hands of surgeons 

^Journal of the American Medical Association, January 20, 1912. 



CHAPTER XXVII. 

INFECTIONS OF AND FROM THE MOUTH, AND 
STERILIZATION. 

The conditions found in the human mouth, as pointed out in 
Chapter III, are of a character which afford lodgement to, and 
opportunities for multiplication of, many forms of bacteria, both 
saprophytic and parasitic. The oral conditions are, however, not 
entirely constant, so that at different periods they may favor the 
development of some special bacterial forms more than others. The 
nature of these variations has not been made out, although their 
effects are indubitable. Again, the oral bacterial inhabitants are 
not constant as to species, for while there are many forms which 
appear to be invariable occupants of the oral cavity, many patho- 
genic forms are but accidental residents. Becoming resident, they 
may or may not develop according as they find in the mouth a suit- 
able soil. The nature of what constitutes a suitable or unsuitable 
soil has not been determined, although in some cases extra- oral 
culture experiments furnish some indications. 

Bacterial growths, as causes of dental caries and diseases of the 
pulp and pericementum, have been discussed in connection with 
those several diseases. It was shown that the pyogenic cocci are 
almost constant inhabitants of the human mouth. There appeared 
also evidence that some important disorders of distant parts are 
directly traceable to septic processes about the teeth, and, in addition 
to these, suppurative diseases in other parts become curable after 
removal of a septic tooth, such conditions representing infection from 
a local dental infection, an important aspect of dental pathology. 

Of the many oral bacterial forms, some are cultivable and some 
are not; hence the specific effects of some are discovered, others are 
doubtful. 

With regard to local affections, other than those described in the 
body of this book, a bacterial causation has been made out in some, 
but in others it has not. 

STOMATITIS. 

Definition. — By stomatitis is meant an inflammation of the mucous 
membrane of the mouth. If secretion is markedly increased it may 
be termed catarrhal stomatitis. 

(766) 



STOMATITIS 



767 



Varieties. — It may be localized, as in marginal gingivitis, or be 
diffuse; and, again, be accompanied by localized tissue destructions — 
ulcerations; the character of the ulceration differs according to its 
probable causes. 

Occurrence. — Most of these diseases belong to the period of child- 
hood, although localized ulcerative stomatitis may appear in the 
adult. 

Causes. — The causes of stomatitis are so many and varied as to 
suggest a classification under heads according to assignable causes. 
While it is true that bacterial infection has not been shown to be a 
direct cause of all of these conditions, some degree of causal relation- 
ship is probable in all of them. The disease may, however, be 
included under two heads according as they are or are not localized, 
and necrotic. The less localized cases appear as a diffuse catarrhal 
affection, affecting wide areas of the oral mucous membrane; the 
others appear as spots of localized tissue destruction attended by 
surrounding hyperemia. 



Catarrhal stomatitis 



Local 



Symptomatic 



Simple. 

Infective 

Eruptive fevers.. 
Syphilis. 
Tuberculosis. 
Typhoid fever. 

Drug action 



Fermentations. 

Diphtheria. 

Gonorrhea. 



Iodids. 
Mercury. 
Lead. 
Pilocarpin, 



etc. 



Ulcerative stomatitis 



Local 



Symptomatic 



Aphthae. 

Thrush. 

Noma and gangrenous stomatitis. 

Herpes. 

Syphilis (primary). 

Gonorrhea. 

Vincent's angina. 

Stomatitis epizootica. 

Actinomycosis. 

Lukwig's angina. 

/ Secondary. 

\ Tertiary. 
Scurvy. 



Syphilis 



Simple Local Catarrhal Stomatitis. — The general symptoms of 
catarrhal inflammation — heat and swelling, with deepened color of 
the mucous membrane, followed by increased secretion and exuda- 
tion — attend several types of oral irritation, such as the irritation 
induced by erupting teeth, particularly of the deciduous teeth. In- 
flammation of any degree may follow the taking into the mouth 
of caustic chemical substances, such as caustic alkalies, mineral 
acids, carbolic acid, etc., which are occasionally taken by children. 



768 INFECTIONS OF AND FROM THE MOUTH 

Other irritant drugs and very hot fluids may produce similar results. 
General catarrhal stomatitis is a frequent affection of confirmed 
smokers, and of drinkers of distilled liquors. 

The cure of these conditions consists in the removal or neutrali- 
zation of the cause, and the use of local, sedatives and antiseptics to 
allay irritation and prevent infection. The most effective method 
of treating the inflammatory condition is by antiseptic sprays, such 
as diluted Dobell's solution, followed by sprays of strong solutions 
of potassium chlorate. If much pain exist, phenol-sodique is an 
admirable sedative antiseptic, used in 10 to 20 per cent, solution, as 
a spray. 

Infective Local Catarrhal Stomatitis. — This in some degree is a 
common, perhaps the necessary, antecedent condition to many of 
the ulcerative forms of stomatitis. It is probable that many of the 
cases of stomatitis found in infants, children, and adults are due to 
unusual fermentations occurring in the mouth. Children whose 
nursing bottles are not kept clean; those who at a later age suffer 
from neglect of the teeth and from the effects of improper food: 
adults in whose mouths dental disease is widespread, and whose 
oral hygiene is very faulty; all exhibit abnormal conditions of the 
oral mucous membrane — more or less swelling, softness, and deepened 
color of the mucous membrane, a coated tongue, and offensive 
breath, with an increase of oral secretions. 

The complexus of oral symptoms is commonly, and also by the 
general practitioner, regarded as symptomatic of gastric, intestinal, 
and hepatic disorders, as doubtless it is, but the causal relation- 
ship is in many cases probably the reverse of that implied in such 
opinions, for it is probable that the disturbances of digestion are 
fermentative in character, and the organisms causing them find their 
way to the stomach from the mouth, which was first affected. The 
treatment of this condition consists in the correction of its causes, 
their non-repetition, and the continued use of oral antiseptics. 

Symptomatic Catarrhal Stomatitis.— Stomatitis in its catarrhal 
form usually accompanies the early and later stages of the eruptive 
fevers, scarlet fever, smallpox, etc. In scarlet fever, smallpox, and 
measles evidences of direct infection of the mouth exist and the in- 
flammatory reaction is pronounced. 

Catarrhal stomatitis is one of the manifestations of secondary 
and tertiary syphilis, antedating the appearance of tissue necrosis 
(ulcerations) . 

More or less catarrhal stomatitis, confined, it may be, to the 
mucous membrane of the gums, is common in the mouths of phthi- 
sical patients; tubercular ulcers may arise or threaten. In some 



STOMATITIS 769 

cases the palate has been perforated. Curtis states that these are 
usually fatal. 

The stomatitis of typhoid fever may be regarded as an almost 
essential feature of the disease. 

The effects of drug elimination by the oral tissues have been 
already discussed (see p. 648 and 773). 

Mercurials in excess produce gingivitis with puffy gums which 
bleed readily; there is coated tongue, fetid breath in marked cases, 
swollen tongue and cheeks, and exfoliation of the teeth. The history 
of administration of mercurials, and, possibly, of syphilis, as a reason 
for it affords a diagnosis. The mercury should be stopped; atropin 
sulphate, 5 minims of a 1 -grain to 1 -ounce solution in water, admin- 
istered as an antisialagogue every four to six hours; a 5 per cent, 
potassium chlorate solution in hydrogen dioxid makes a useful 
mouth wash for reducing the local inflammation. 

Ulcerative Stomatitis. — In all probability these ulcerations are 
always infective. Like catarrhal stomatitis the ulcerative disease may 
have only a local significance or be indicative of some general disease. 

Ulcerative Stomatitis of Local Significance. — The more usual or 
infantile forms of these disorders are a sequel of catarrhal stomatitis, 
at least of an acquired debility of the oral tissues, and their primary 
cause is, therefore, the cause producing a condition of mucous mem- 
brane which permits the growth of infective organisms. One of these 
diseases, thrush, has already been described. The others, aphthae, 
herpes labialis, and noma, are all probably due to the action of 
organisms. 

Aphthae. — This affection is common in its isolated form, as the 
canker sore. In the catarrhal stomatitis of children, during or after 
dentition, multiple sores frequently make their appearance. The 
condition can best be studied when it appears as an isolated sore in 
the mouth of the adult. The most common situation of the sore is 
at the junction of two mucous surfaces, such as that of the gum with 
the lip or cheek, or that of the floor of the mouth with the gum or 
tongue. Redness diffused over a limited area, followed by a nodular 
hardening, occurs, during which local pain is annoying; the centre 
of the hardened area breaks, the epithelium disappearing, forming a 
raw surface, which quickly acquires a rough, yellowish white coating 
which is easily removable. The sores are very painful. 

The mouth is usually otherwise healthy, and there is an absence 
of associated throat and skin affections. 

•The notable fungus of the blastomycetes is the saccharomyces 
albicans; this organism, when classified by mycologists as a thread 
fungus, was known as the oidium albicans (Fig. 705). The growth 
49 



770 



INFECTIONS OF AND FROM THE MOUTH 



of this organism illustrates forcibly the influence of soil on the 
growth of fungi. It does not occur in the mouths of healthy, well- 
nourished, and clean children with good surroundings. It is a disease 
of childhood, particularly of nurslings, and -its occurrence is almost 
always confined to bottle-fed babies whose feeding bottles are kept 
in an unclean condition. Debility of the oral tissues is established 
in consequence of the fermentations arising from the source just 
named, furnishing a favorable condition for the development of the 
saccharomyces (oidium) albicans. The condition produced is known 
as thrush. The infection may be carried from one child to another, 
and if the fungus be brought in contact with an abraded mucous 
surface of an adult it may develop. 

The fungus burrows between the epithelial cells of the mucous 
membrane (Fig. 706), not beyond it. It first appears in small spots 
which coalesce, until large patches of a membranous-like growth 



Fig. 705 



Fig. 706 




Saccharomyces albicans, thrush fungus. 
(Miller.) 

cover extensive surfaces, spreading 
by continuity to all of the mucous 
surfaces associated with the mouth. 

As bud fungi flourish only in 
media of acid reaction, the use of 
alkaline washes is indicated in 
the treatment of this condition. 
Wiping the patches with dilute 
phenol-sodique is efficacious. Small 
spots may be cauterized with silver 
nitrate or trichloracetic acid. 

Hydrogen dioxid or 25 per cent, 
iodin in glycerin are also useful. 

This condition follows so constantly upon the taking of very 
indigestible food, such as lobster, Welsh rarebit, etc., that acute 
indigestion must be regarded as having some causal relationship 




Pavement epithelium covered with 
spores of the oidium albicans. (Ch. 
Robin.) 



STOMATITIS 771 

w ith it. It is also of frequent occurrence in the mouths of dyspeptics; 
that form of gastric disturbance attended with a deficiency of hydro- 
chloric acid in the gastric juice appears to have a constant association 
with it, though it is probably caused by the oidium albicans. 

The appearance of ulcerative stomatitis in children, together with 
its treatment, was discussed in the chapter on Dentition. 

The general treatment of these ulcerations appearing in the mouths 
of children is the administration of a laxative, and the subsequent 
administration of listerine, gtt. x, every two hours. Locally the 
mucous membrane is to be sprayed with hydrogen dioxid, followed 
by sprays of strong solutions of potassium chlorate. 

Localized aphthous patches in the adult are promptly relieved by 
the administration of calomel, gr. ij, at night, followed in the morning 
by a mild saline. The local sore is dried and touched with pure 
carbolic acid. The administration of alkalies before meals, and 
hydrochloric acid after meals, usually remedies the gastric condition, 
unless it be of long standing. A variety of aphthous sore is called, 
from the anatomical situation of the ulcers, follicular stomatitis. 
Irritation and swelling of the mucous follicles in the palatal, 
buccal, and labial mucous membrane are accompanied by more or 
less localized inflammation; the follicles become ulcerous, the small 
ulcers having a uniform size. This condition quickly disappears 
under the treatment advised for ulcerative stomatitis. An indica- 
tion of the bacterial origin of all of these disturbances is seen in 
the efficacy of antiseptics used in their treatment. 

Rubber Sore Mouth. — A form of stomatitis is due to artificial 
dentures resting upon the mucous membrane, and either by pressure 
or light' friction, or possibly by preventing radiation of heat, they 
cause desquamation of the epithelium. The part beneath the plate 
assumes a more or less reddened or ulcerated appearance. Vulcanite 
plates that are not smooth upon their surfaces of adaptation may 
produce this physical irritation, but oftentimes such surfaces may 
covered with infective mucous plaques, so that this may in some 
cases be an added cause. 

Eilestein has shown that the use of vermillion colored vulcanite 
causes minute pores to appear in the vulcanite which harbors bacteria 
which may induce inflammation of the oral epithelium. 1 The use of 
carmine-colored vulcanite is suggested. 

Treatment. — The treatment consists of rest and healing mouth 
washes. Antiseptics are usually included. (See Gingivitis.) 

'Stomatitis Aphthosa Epizobtica. 2 — This is the oral expression 
of foot-and-mouth disease occurring in cattle and rarely fatal, and 

1 L'Odontologie. See Dental Cosmos, February, 1911, p. 248. 

2 Lartschneider: Dental Cosmos, 1908, p. 880. 



772 INFECTIONS OF AND FROM THE MOUTH 

usually lasting about eight weeks. The germ is not fully determined 
as yet. 

Equinia (Glanders) . — An infectious disease of cattle which may be 
transferred to man, producing a purulent discharge from eyes, nose, 
and mouth. 

Diagnosis. — The diagnosis rests upon the presence of the disease in 
nearby cattle and the prodromata and later presence of fever, pustules 
on the mucous membranes of the lips, tongue, and sometimes on 
the hard palate and throat, occasionally between fingers, around 
nails, or on nipples. These later burst, leaving ulcers with a grayish- 
yellow coating. The pustules dry up without scars in the second week. 

Treatment. — The treatment rests upon antisepsis in so far as the 
local manifestations are concerned. 

Diphtheria. — While the point of first attack of the diphtheria 
bacillus is most marked about the soft palate and tonsils, the false 
membrane forming there and spreading to the pharynx,. more or less 
general inflammation of the oral mucous membrane also occurs. 

NOMA, CANCRUM ORIS, GANGRENE OF THE MOUTH. 

In ill-fed, ill-nourished, and ill-kept cachectic children, the debili- 
tation of the oral tissues may exceed the grades given, and a disease, 
probably bacterial in origin, may arise which leads to widespread 
necrosis of the cheeks and maxillse. The condition is called gangrene 
of the mouth, noma, or cancrum oris ; the latter term has been applied 
to the less severe varieties. 

This disease may make its appearance as an ulcer at the junction 
of cheek and gum; in other cases a severe stomatitis arises without 
a primary ulcer. A greater or less extent of the cheek acquires a 
board-like hardness, becoming livid; the overlying mucous mem- 
brane breaks, exhibiting a large slough. The necrosis extends toward 
cheek and jaw, destroying further tissue. The sloughs undergo 
putrefactive decomposition, emitting a stench. The destruction of 
tissue may be arrested, or may proceed, destroying in a few days 
the entire cheek and bony tissues. In the more severe cases the 
disease is almost invariably fatal, because the extent of the tissue 
destruction bears a constant relation to the underlying debility of 
the patient. It will be seen that the disease resembles malignant 
pustule or carbuncle in several of its features. 

Schimmelbusch 1 found a bacillus (pure culture) upon the borders 
of the necrosis w^hich may' prove pathogenic of noma. 

1 Miller: Dental Cosmos, September, 1891. 



NOMA, CANCRUM ORIS, GANGRENE OF THE MOUTH 773 

Hillesen obtained a diplococcus which developed in pure culture, 
produced noma in an animal into which it was injected, and from 
the lesion a pure culture of it was obtained which in like manner was 
put through four animals. 1 

These cases are purely medical; so that their full discussion is not 
warranted in these pages. The principle of treatment is to improve 
the general condition of the child, destroy the probable infection 
in the borders of the still vital tissue by cauterization, and promote 
sloughing of the necrosed tissue by the use of antiseptic applications. 

Fig. 707 




Noma. (J. Lewis Smith.) 



Dr. L. Fisher (Xew T York) reported a case upon the inside of the 
cheek, cured by applications of ichthyol in lanolin four times a day 
over the entire area. 2 

The Eruptive Fevers. — Hyde and Montgomery describe the fol- 
lowing oral symptoms associated w T ith various diseases having 
eruptive dermatitis as phenomena : 

Scarlatina. — The mucous surfaces of the mouth and fauces are 
engorged tumid, reddened, and often covered with deep reddened 
puncta. The tongue is coated w T ith a white fur over the filiform 
papilla?. This is first partly lost, giving red puncta and a white 
background; when totally lost it gives "strawberry tongue." 



1 Dental Cosmos, 1908, p. 180. 



2 Ibid., 1902. 



774 INFECTIONS OF AND FROM THE MOUTH 

Variola. — The papules may appear over the entire alimentary 
canal. In the mouth they lose their epithelium, through heat, 
moisture, and friction. Reddened excoriated surfaces appear, over 
which the epidermis is reformed. Gangrenous complications are rare. 

Hemorrhagic Variola (Effusions of Blood into Mucous Surfaces). — 
The mucocutaneous orifices are crust-covered and exude an extreme 
fetor. Blood may escape from the mouth. 

Varicella. — The macular lesions may extend to the surfaces of the 
eyes, mouth, etc. 

Rubeola. — Even three days before skin eruptions. "Koplik's spots," 
bluish white or bright red with central bluish-white punctum on 
mucous membrane. In period of affloresence a catarrhal or eruptive 
inflammation. 

Syphilis. — Secondary eruptions, later forming mucous patches; 
characteristic crusts about nose and mouth. 

Urticaria. — The eruption in well-marked cases may include the 
mucous membranes. 

Angioneurotic Edema. — The rosy red to livid edematous plaques 
may appear upon the lips and pharynx, producing at times dyspnoea. 

Erythema Scarlatiniforme. — The mucous membranes in mouth 
and fauces may be reddened or be denuded of epithelium, but the 
characteristic "strawberry tongue" of scarlatina is wanting. 

Erythema Iris. — The papules may coalesce and be filled with 
blood or hematuria may result with severe involvement of mucous 
membranes of lips and mouth, ulceration rapidly ensuing. 

Erythema Multiforme. — Like the iris variety the macules may appear 
in the mouth. 

Dermatitis Herpetiformis. — When affected, mucous membrane of 
mouth sodden, macerated, pustules; and bulla? form and rupture, 
leaving raw erosions or sloughing patches of mucous membrane; 
extremely foul odor. 

Herpes Simplex. — Herpes Zoster.— See this chapter. 

Erysipelas. — May extend to mouth, causing a dry, tumid, glazed 
appearance. 

Rhinoscleroma. — A rare disease; usually begins in nose; may extend 
to mouth, with ulcerative destruction, causing exfoliation of the teeth. 

Pemphigus Foliaceus. — The mucous membrane of the mouth and 
throat may be denuded. 

Pemphigus Vegetans. — White patches followed by excoriation with 
foul odor may occur. 

Drugs Producing Stomatitis. — Many drugs taken internally may 
produce dermatitis or stomatitis as a temporary efflorescence, while 
with some, as mercury, the impression is more profound (see p. 648) ; 



SYPHILITIC AFFECTIONS OF THE MOUTH 77o 

with others it is simply expression of idiosyncrasy, with which the 
oral tissues may or many not take part. 

Iodin or bromin or their compounds; antipyrin and others of its 
class; arsenic, belladonna, aconite, carbolic, nitric, tannic, boric, and 
benzoic acids; sodium benzoate and sodium borate. 

Chloral, digitalis, mercury, opium and its alkaloids, phosphorus, 
podophyllum, potassium chlorate, castor oil, cinchona and its alkaloid, 
quinine, salicylic acid and salicylates, strychnine, tar, turpentine, and 
others of less .interest are mentioned. Silver nitrate may produce 
argyria of the skin and mucous membranes. As instanced by argyria, 
the drug finds its way to the superficial tissue in which it may 
produce irritation. 

SYPHILITIC AFFECTIONS OF THE MOUTH. 

The recognition of syphilitic lesions about the mouth is of vital 
importance to the dental operator, first, because by the recognition 
he may take steps to prevent the carriage of infection to innocent 
patients; and secondly, that he may avoid inoculation of himself 
by the poison. 

In the minds of many, syphilis is associated with the lower class of 
persons, who are confirmed debauches. ^Tiile it is undoubtedly true 
that its prevalence is most marked in this class of persons, it appears, 
with horrible frequence, in persons who would be little suspected 
of having such infection. The operator is to be guided in his opinions 
and precautions in this matter, not by the social status of the patient, 
but by the nature of the morbid conditions existing. 

The cause of syphilis is the traponenia pallidum discovered by 
Schaudin and Hoffman, and present in its lesions, transmitted from 
one person to another directly or through the medium of an inani- 
mate object which has been infected. 

The diagnosis may be made by microscopic examination. The 
sore is washed and the serum later exuded used to make a smear on 
a glass slide. Stein states that the edge of the sore should be scraped 
with a sharp instrument after washing, and the serum collected 
from that source, otherwise the treponema may not be obtained. 1 
This is first dried in the air, then stained with Hastings' stain. After 
a minute distilled water is added until a metallic film is formed. 
After five minutes more they are washed in running water and 
dried. The treponema pallidum stains a faint blue. 2 They may 
also be seen living by aid of the "dark-field illuminator." 

1 Dental Cosmos, July, 1913, p. 744. 

2 McKee: Dental Cosmos, 1909, p. 1437. 



776 INFECTIONS OF AND FROM THE MOUTH 

Syphilis is usually divided into three stages, primary, secondary, 
and tertiary; to these may be added a fourth stage, viz., in patients 
who have been discharged as cured mild manifestations of disorders, 
particularly of the skin and mucous membranes, make their appear- 
ance from time to time, and disappear promptly upon the adminis- 
tration of iodids. The semen of syphilitics in the secondary period 
is infectious to apes. 

The first stage of syphilis — primary syphilis — consists in the for- 
mation of the primary sore or chancre, and the involvement of the 
nearest lymphatic glands. Secondary syphilis is attended by fever, 
eruptive inflammations of the skin, inflammation and superficial 
ulceration of mucous structures. In tertiary syphilis destructive 
inflammation of the skin, mucous membranes, and connective tissue 
occurs, together with the formation of specific tumors — gummata. 

Some differences of opinion exist among syphilographers as to the 
relative infective power of the secretions from the several lesions 
of syphilis. All are agreed, however, that the secretions from the 
secondary lesions observed in and about the mouth are highly 
infective. It is the part of prudence to regard all syphilitic lesions 
as infective. All these stages of syphilis may be seen in the human 
mouth. It is to be remembered that if the mucous membrane of 
the mouth be infected from a mucous patch (a secondary lesion), 
the acquired disease will appear, not as a mucous patch, but as a 
chancre. It is from mucous patches that infection is most to be 
feared. 

Primary Syphilis of the Mouth. — Causes. — The primary lesion of 
syphilis, chancre, when found in the mouth is a consequence of direct 
infection from a syphilitic. The infection occurs from contact 
of the mucous surface of the mouth with a syphilitic lesion upon 
another person. It has been transmitted by kissing, even with 
an innocent person as the intemediary; it may occur from using 
a glass or cup previously used by a syphilitic, by smoking cigars or 
cigarettes which have been made by syphilitic cigarmakers, who 
have applied the tongue to the tobacco in attaching the wrapper. 
Dental instruments may be the carriers. Any of the articles named, 
or the contact of any article which has been in contact with a 
syphilitic lesion, if brought in contact with an abraded mucous sur- 
face, may cause infection. 1 

The infection may be transferred from patient to operator if the 
fingers have any abraded surface, or if the surface is broken acci- 

1 Metchnikoff and Roux found that an ointment composed of 10 parts calomel 
and 20 parts lanolin, applied by inunction to an intentionally infected part, prevented 
the appearance of syphilitic infection if used within one hour after inoculation. Mer- 
curic chlorid was of no avail. Dental Cosmos, 1907, p. 1007. 



SYPHILITIC AFFECTIONS OF THE MOUTH 111 

dentally by an instrument. Dentists have been inoculated upon the 
hand. During and since the time of Hunter the use of teeth from 
syphilitic patients in plantation operations has been a clearly 
recognized medium of communication. About 32 per cent, of all 
primary chancres appear within the dental field either upon the 
lips or within the mouth. 

Appearance and Diagnosis. — "The primary lesion of syphilis 
never makes its appearance before ten days after infection; the 
maximum period is about ninety davs; the average is twentv-one 
days." 1 

It usually appears as a single, elevated, hard papule. In cases of 
dental infection, most frequently about the lips, the papule loses its 
epithelial coating after some days. The induration surrounding the 
papular mass increases until the papule, which is now raw and in a 
process of ulceration, appears surrounded by a ring of cartilaginous 
hardness. This induration is the one distinguishing feature of the 
chancre, which is not painful. In about a week after the appearance 
of the primary sore, swelling of the submaxillary lymphatic glands is 
observed. In case the chancre appears upon the tongue, the sub- 
hyoid lymphatic glands are swollen. 2 Unless pyogenic infection has 
occurred, the lymphatic involvement is not inflammatory, there 
being no pain present. In from three to four weeks the sore disap- 
pears, leaving no signs of its site in some cases; in others, some 
induration may persist. 

The diagnosis of this condition is the important consideration, so 
far as the dental practitioner is concerned, its treatment being the 
province of the medical practitioner. 

The elevation of the sore, its induration, and, if obtainable, the 
time of inoculation, are diagnostic data. The sore is single, as a 
rule, and there is hard, nodular painless swelling of the neighboring 
lymphatics. A single ulcer of ulcerative stomatitis may in some 
degree simulate the appearance of a very small chancre. It may 
exhibit slight induration, but its irregular form, situation, painful- 
ness, and the usual absence of lymphatic involvement, together 
with its prompt disappearance after sterilizing the mouth and cauter- 
izing the ulcer, will differentiate the two sores. If the chancre be 
upon the tip or sides of the tongue, where it is subjected to irrita- 
tion, it may become very large and bear a close resemblance to 
epithelioma of that organ. In epithelioma there are apt to be pains 
of a lancinating character, the induration follows ulceration, and 
the ulcer has hard edges and often a warty-like growth. 

1 Gross: System of Surgery. 2 Park: Surgery 



778 INFECTIONS OF AND FROM THE MOUTH 

It is a wise precaution to view all sores about the mouth as possibly 
infectious. All errors of diagnosis in this direction will be more than 
compensated for by the assurance of non-transference of infection. 

Secondary Syphilis of the Mouth.— The secondary manifestations 
of syphilis may be observed in and about the mouth, no matter what 
the location of the primary lesion may have been ; they are the result 
of a general, not a local, infection. A skin eruption appears also. 

Fig. 708 




Chancre of J;he lip. 

Secondary infections of the mucous tissues appear in from four 
to twelve weeks after the appearance of the primary lesion. Sore 
throat, due to inflammation of the mucous membrane of the pharynx 
and parts about, is almost constant; together with syphilitic hoarse- 
ness, due to the extension of the affection to the mucous membrane 
of the larynx. 

The appearance of copper-colored areas upon some portion of the 
mucous membrane, on the tonsil, pharynx, soft palate, lips, or bucco- 
labial surface, precedes the loss of epithelium over these surfaces, 
which soon occurs, forming the most virulently contagious lesion 
of syphilis, the mucous patch. The patches become covered with 
a grayish-white, opalescent, pasty covering, resembling the ulcera- 
tions of non-specific stomatitis. So close is the resemblance that a 
differentiation can only be made at times by additional evidences of 
secondary syphilis. Single patches may coalesce, forming large, 
irregular areas covered by a grayish-white pellicle. These patches 
are rarely painful. Ulcerations having ragged, irregular outlines 
may appear at the sites of. the original patches or in other situations, 
and exhibit a tendency to spread. In healed cases the cicatrices 
present a whitish pellicle and contracted scar, indicative of old 
healed ulcers. In the skin little pits and linear scars are symptomatic. 

The diagnosis of the condition is determined by the history and 



SYPHILITIC AFFECTIONS OF THE MOUTH 779 

by a discovery of other lesions of secondary syphilis, iritis, head- 
ache, neuralgia, paralysis of muscles of eye and face, chorea, brittle, 
cracking nails are often early symptoms; 1 also the lymphatic glands 
will be involved; skin eruptions, falling out of the hair (alopecia), 
and the areas of copper-colored eruption upon the mucous mem- 
brane of the pharynx and soft palate. 

Hugenschmidt- has observed among syphilitics, who presented no 
local lesions, the frequent nocturnal occurrence of indefinitely located 
dental pains, spreading to the palatal region. In case of doubt, 
search for the treponema, or the Wassermann or luetic reaction may 
be employed. 

Tertiary Syphilis of the Mouth. — The syphilides of the secondary 
stage arise in, and are confined to, the mucous and dermal structures; 
those of the tertiary stage arise in the deep connective tissues, and 
are frequently associated with periosteum. 

Tertiary lesions, as seen by the dentist, are usually in the form of 
ulcers of, first, the soft or hard palate, and of the tongue or lips. In 
the earlier stages hard, nodular formations may be noted as ante- 
cedents to the ulcerations. Chronic periostitis of the palatal processes 
may occur, leading to the formation of localized thickenings. In 
other cases, in the soft palate, upon the tongue, or in the hard palate, 
localized swellings may occur, having a livid red appearance; the 
overlying mucous membrane breaks, establishing an ulcer, which 
may perforate the soft palate and destroy a portion of the palatal 
process, or form large ulcers on the tongue. The condition is one 
of gumma. These lesions appear in from two to five years after the 
secondary manifestations. 

Tertiary Lesions. — The sight and hearing may be affected, the 
throat diseased, causing loss of voice, necrosis of the bones and tissues 
of the nose causing deformity. The brain or spinal cord affected 
may cause paralysis, locomotor ataxia, or loss of reason. These are 
usually the result of failure to follow treatment to a conclusion. 

The tongue may have either a localized or widespread parchment 
like hyperplasia of the mucous membrane, and muscular tissue which 
may cause it be become indented by the teeth, to lose its papillae, 
and become dry and red. Pedersen 3 calls attention to the fact that 
the indentations do not disappear when the tongue is stretched, 
while if due to ordinary debility they may do so. 

Although there is much doubt as to the degree of infectiveness of 
these tertiary lesions, precautions as to sterilization should be taken 
as with the primary and secondary lesions. A defined, ragged ulcer 

1 E. Whitney: Dental Cosmos, 1911, p. 524. 2 Dental Cosmos, 1892. 

3 Ibid., 1908, p. 332. 



780 INFECTIONS OF AND FROM THE MOUTH 

occupying the hard or soft palate, which has persisted for a long 
time, should always be viewed with suspicion, and a search be made 
for other evidences of syphilis. 

These ulcerations appearing upon the side of the tongue may 
closely simulate epithelioma of that organ. The confusion is increased 
if, in consequence of the presence of jagged teeth, a continuous 
irritation is excited. Moreover, leukoplakia of the cheeks, a diag- 
nostic sign of incipient epithelioma, frequently accompanies tertiary 
syphilis. 

The existence of tertiary syphilis is of great clinical importance to 
the dentist in that a condition of lessened resistance of tissues is 
established, and disease processes which in the healthy person are 
comparatively circumscribed, in the syphilitic run a riotous course. 
A septic pericementitis by extension may involve a wide area of 
periosteum, leading to extensive maxillary necrosis. 

Treatment. — The treatment of syphilis has been largely by the 
administration of mercury and potassium iodid for a long period 
until the treponemata shall have been killed out. If not so con- 
tinued the tertiary lesions may reappear with serious results The. 
latest development in treatment is the use of Ehrlich's preparation 
of arsenic, dioxydiamedoarsenobenzol, "606," or "salvarsan," for 
which positive claims as a prompt cure are made. 

TUBERCULOSIS OF THE MOUTH. 

The bacillus of tuberculosis, under favorable conditions, develops 
in the tissues of the mouth, producing its characteristic lesions. 
Finding a suitable soil, such as is furnished by the heredity which 
predisposes to phthisis pulmonalis, the bacillus may find entrance 
to the deeper tissues from the mucous membrane of the mouth and 
excite tuberculosis in the deep structures, the bone, etc. A number 
of perforations of the hard palate have occurred. According to Curtis 
these are usually fatal. What part is played by local oral and dental 
lesions in tuberculosis of distant parts, by establishing pathways 
for the entrance of the bacilli into the circulation, is at present 
conjectural, but that such infections occur is very probable. Lupus, 
a skin tuberculosis, may extend to the mouth producing nodules. 

ACTINOMYCOSIS. 

The condition produced by the development of the ray-fungus, the 
actinomycosis, in the lower jaw and cervical regions of cattle and 
swine — lump-jaw — is not unknown in human beings. It may be 



GENERAL SEPTIC DISEASES OF DENTAL ORIGIN 781 

(1 by chewing straw or grass in which the ray-fungus has 

} ;d "rust." 

r 1 gives 203 cases reported in German medical literature 
be -n 1886 and 1891'. In at least 120 of these cases the point of 
entrance of the fungus was found to be in the region of the mouth or 
throat. Actinomycosis threads have been repeatedly found in the 
saliva and in carious teeth, and notably in the tonsils. Whether the 
path of entrance to deeper structures is ever through carious teeth 
is undertermined, but certainly lesions or wounds about the mouth 
furnish an entrance. Padgett reports a case of alveolar ulceration 
following extraction, which proceeded to abscess upon the face. 
Bacteriological examination showed the ray-fungus. 

The disease has yielded to the action of sulphate of copper, -§- 
grain, plus iodid of potassium, 10 grains, internally four times a day, 
together with local irrigation of 0.1 per cent, solution of copper 
sulphate. 2 

GONORRHEA. 

Cases of oral infection by the gonococcus of Neisser have been 
reported. The oral mucous membrane and the gums may undergo 
intense suppuration w T ith its accompaniment. Fever and its accom- 
paniments may be present. The eyes are very subject to secondary 
infection in an individual suffering from gonorrheal urethritis. The 
hands are a medium of transference. Babes may be directly infected 
by the mother during birth, and blindness often results. The law 
now requires the instillation of a mild solution of silver nitrate or 
other antiseptic as advocated by Crede. The diagnosis can be made 
by microscopic examination of the bacteria. Stein claims that 
endeavor to infect the nose with gonococci failed and questions oral 
infection by them. (See p. 677.) Lederer in a case of oral infection 
in a patient with urethral gonorrhea found it by microscopic exami- 
nation to be a case of Vincent's angina, which see. 

GENERAL SEPTIC DISEASES OF DENTAL ORIGIN. 

The effect of the existence of dental diseases upon the body at 
large, particularly as regards secondary infection, is a matter increas- 
ing in importance as the possibilities of their connection are made 
out. At present the organisms of greatest demonstrable pathologi- 
cal interest are the pyogenic cocci. The almost constant presence 

1 Dental Cosmos, 1891. 2 Brophy: Dental Cosmos, 1908, p. 78. 



782 INFECTIONS OF AND FROM THE MOUTH 

of these organisms in the mouth, carried thence into the pharynx, 
posterior nares, larynx, lungs, and stomach, furnishes the reason for 
the pyogenic and phlegmonous inflammations which occur in these 
organs. The diplococcus of pneumonia, a frequent organism, but 
waits a favorable opportunity to establish high inflammations and 
fibrinous exudations in the lungs, and possibly in other structures. 

The most important clinical associations of dental with general 
infections are diseases of the pericementum. The pulps of teeth, 
having no lymphatics, do not appear to take up and transmit the 
products of the action of septic organisms; but while the evidences 
of such absorption, involvement of the neighboring lymphatics, are 
not present, it must be remembered that the veins may transmit 
the poison, and, in addition, may perhaps convey organisms from a 
diseased but still vital pulp to distant parts. When, however, the 
pulp is dead and the pericementum is invaded, there is no doubt of 
general infection from this local source. More or less septic intoxica- 
tion is a common attendant upon severe septic apical pericementitis, 
and septicemia accompanied by inflammation of the neighboring 
lymphatic glands is of sufficient frequency to emphasize the need 
of the vigorous antiseptic treatment recommended in all of these 
cases. 

Pyemia is far more uncommon. 1 Pyogenic organisms, gaining 
access to the blood current from the local source of infection, establish 
suppuration in distant parts; in other parts of the bone, or in other 
bones (osteomyelitis), in the lungs, meninges, and substance of the 
brain. One case 2 has been reported where abscess of a toe, ear, and 
forearm ceased, and recovery took place after treatment and filling 
of septic root canals. Several cases are tabulated by the same author 
in which extensive necrosis and death resulted from pyemic infec- 
tion from septic pericementitis. Some of these cases recorded were 
associated with acute, some with chronic, septic pericementitis. 

In addition to the usual pyogenic cocci, Miller has isolated several 
forms of cocci, bacilli, and spirilla, forming products which, if injected 
into the circulation of animals, cause death from septicemia in from 
hours to days. As many of these forms may be brought into rela- 
tion with deep parts by the anatomical conditions created by pulp 
death, the possibilities of many types of infection via pulpless teeth 
are evident. 

The possibilities of local as well as general infections through the 
conditions established in the several forms of pyorrhea alveolaris 
should not be forgotten. (See pp. 438, 603, 605, 631, 742, 787.) 

1 Miller: Dental Cosmos, 1891. 2 Ibid. 



LEUKOPLAKIA BUCCALIS 783 

The pockets formed by the soft tissues overhanging lower third 
molars whose eruption is impeded invite the passage of septic organ- 
isms to deep parts. Local pyogenic infections are common in these 
cases, and may extend into the pharynx and the submaxillary tissues, 
as in Ludwig's angina. 

HERPES LABIALIS (HERPES SIMPLEX). 

This consists of a vesicular eruption upon the lip, tongue, mouth, 
cheeks, or allse of the nose. The vesicles are filled with a clear fluid 
which soon discharges. An excoriation is left often covered by a 
light crust, which is never followed by a scar. The condition may 
cause little pain or considerable burning and itching. It may accom- 
pany colds, fevers, exposure to heat, draughts, and gastric disorders. 
It follows either a direct irritation of the nerves, as after the use of 
rubber dam or other dental operations in susceptible persons, or may 
be of reflex origin; in either case localized peripheral neuritis being 
the initial lesion. 1 There is some reason to believe that infection 
plays a part in its production. As a preventive it is w T ell to lubricate 
the lips with glycerin and rose water or with cold cream when much 
stretching or other irritation is necessary. 

HERPES ZOSTER. 

This is a probably infectious disease, almost invariably mono- 
lateral, associated with a neuritis usually, of a spinal ganglion or with 
a peripheral neuritis, which produces, first, a hyperesthesia of the 
integument, macules, and later vesicular eruptions not usually 
beginning on a mucous surface. They appear in groups and may 
coalesce, forming patches. Desiccation forms a crust; pus may 
form. 

The interest to dentists lies in the fact that in zoster of the head 
exfoliation of the teeth is said to be associated in rare cases. 2 

LEUKOPLAKIA BUCCALIS. 3 

Upon the inner surface of the cheeks or lips, and upon portions of 
the gum and the dorsum and edges of the tongue, may appear sharply 
outlined, dull, whitish, slate-colored or silver-whitish points, disks, 
streaks, bands, ribbons, or patches of irregular shape, either flattened 
pr slightly elevated, above the general level of the mucous surface. 
They may crack or fissure, and inflammation of the derma and pain 

1 Hyde and Montgomery: Diseases of the Skin. 2 Ibid. 3 Ibid. 



784 INFECTIONS OF AND FROM THE MOUTH 

result. Ordinarily they are simply rough and without much dis- 
comfort. It occurs almost exclusively in males. They differ from 
the mucous patches of syphilis in that the latter are soft and tend to 
ulcerate, and, while they may accompany syphilis, may occur in its 
absence or of any history of it. 

They simulate the keratosis of lichen planus, which should also 
appear as papules upon other parts of the body. 

Apart from syphilis, it is due to irritation such as that from 
tobacco or rough teeth, and with syphilis, tobacco, and rough teeth 
may be additional excitants. 

R. H. Ivy reports three cases with tendency to epitheliomatous 
degeneration, all without history of syphilis, and in two of which 
the Wassermann reaction was negative. 1 

The use of alcohol and spices are also a cause. 

The pellicle is closely adherent, and consists of an hypertrophied 
and hyperkeratinized epithelium, with more or less inflammatory 
infiltration of the derma and with partial obliteration of the papillae. 

The chief danger in the disease is the tendency to epithelioma, 
some authors estimating 30 per cent., especially in the cases in which 
exfoliation and ulceration occur. Some fourteen years ago a male 
patient presented with a leukoplakia in which there was a constant 
desquamation as though very hot liquids had been used. Medical 
treatment was given, tobacco and liquor were largely avoided, but 
after about twelve years, epithelioma involving a jaw operation 
occurred. 

The removal of the pellicles by suitable caustics, galvanocautery, 
or bur, and radiotherapy, the use of soothing mouth washes, together 
with a hygienic regimen, and the avoidance of irritants like tobacco, 
alcohol, spiced, hot, or iced foods, is the usual treatment to avoid 
epithelioma. The diagnosis lies clearly within the province of the 
dentist who may note it before the patient. The treatment is 
usually conducted by the physician, and is often unsatisfactory as 
to permanent cure. Cases with syphilitic history, of course, require 
antisyphilitic treatment. 

Leukoplakia has been also called buccal psoriasis, but psoriasis 
does not affect mucous surfaces, hence it is a misnomer. 

LICHEN PLANUS. 

This condition, which may simulate leukoplakia, 2 is characterized 
by an eruption consisting of glistening flat-topped polygonal papules 

1 New York Medical Journal, October, 1912, p. 1187. 

2 Ibid., April 13, 1912. 



PHOSPHOR NECROSIS 785 

with tendency to form irregularly arranged groups. On the mucous 
surface they appear as whitish macules, striae, or flat papules on both 
sides of the tongue at the points in contact with the molar teeth. 

They are the result of an arterial or venous hyperemia of the 
papilla* of the corium, a secondary thickening of the lower part of 
the rete, and a tertiary flattening of the papule by pressure. 

A proliferation of cells in the granular layer and a deposit of 
keratohyalin in whitish spots occur. This causes a similarity to 
leukoplakia. It usually occurs in the nervously exhausted, though 
many patients may have a fair degree of body nutrition while yet 
nervously exhausted. 

PHOSPHOR NECROSIS. 

This disease is a more or less extensive necrosis of the maxillae due 
to the entrance of phosphorus or its fumes into contact with the 
periosteum or pericementum of a tooth. 

It was formerly frequent in match factories, when white phosphorus 
was used, though now less when the red is employed, but has occurred 
through the chewing of match heads, and a case has been reported 
in which a half grain taken in three days caused it. 1 

As it does not ordinarily occur in the mouths of those having 
sound teeth, it is generally regarded as of local origin, the phosphorus 
gaining entrance either through the pulp canal of a tooth, or, possibly, 
through some point of injury external to the tooth. 

Abscesses containing offensive pus cause great swelling and exces- 
sive salivation, and may cause several fistulae, while the swallowing 
of the discharge causes general toxic disturbance, and infection such 
as pneumonia or cerebrospinal meningitis may have rapid effect. 

The periosteum remains unaffected as to its vitality, while the 
bone proper undergoes osteoporous necrosis, becoming like rotten 
sponge. As the sequestrum is separated, there is a tendency to 
formation of new bone by the periosteum. The necrosis of bone may 
be very extensive, involving in the lower jaw the entire horizontal 
portion, while the ramus may remain unaffected. In the lower jaw, 
after exfoliation, the bone may be almost entirely restored to an 
amount nearing fair comparison with the ordinary edentulous 
mouth, while in the upper jaw no repair occurs. This new bone may 
undergo atrophy if not put to work by artificial teeth. 2 As a pro- 
phylactic sodium bicarbonate solutions are recommended by Arnone. 3 

* 1 Arnone: Dental Cosmos, 1910, p. 425. 

2 For consideration of treatment the reader is referred to Garretson's System of 
Oral Surgery, sixth edition, and other writings upon the subject. 

3 Dental Cosmos, 1909. 

50 



786 INFECTIONS OF AND FROM THE MOUTH 

SCORBUTUS. 

This is scurvy as described on pages 215, 649, 684, and below. 

PURPURA HEMORRHAGICA. 

This is the appearance of small purplish spots beneath the skin 
and mucous membrane, and is dependent upon infection and toxic 
conditions. 

Brown, 1 following Schamberg, presents the following clear differ- 
ential symptoms: 

Scokbutus. Purpura Hemorrhagica. 

1. Occurs in those subjects due to lack 1. No such etiological relationship. 

of vegetable food and to bad hy- 
giene. 

2. Definite antecedent symptoms, weak- 2. Antecedent signs slight or absent. 

ness, impaired circulation, etc. 

3. Onset slow. 3. Onset sudden. 

4. Gums spongy, swollen, and bleeding; 4. Gums often bleeding, but not swollen. 

teeth loose. 

5. Severe muscular pain. 5. Less marked. 

6. Brawny infiltration of lower extremi- 6. Not present. 

ties. 

7. Hemorrhages from mucous mem- 7. Hemorrhages from mucous mem- 

branes, not profuse, as a rule. branes so severe as to sometimes 

prove fatal. 

LEPROSY. 

During the progress of leprosy, an infective disease, characteristic 
nodules and ulcers appear about the oral structures. As many parts 
of the head are affected in like manner, these are but symptoms of 
the progress of the effects of the Bacillus lepra. 2 

ANGINA. 

Angina is usually defined as a sense of choking or suffocation, 
a symptom which accompanies inflammatory affections of the 
pharynx as well as the paroxysmal neuralgic affection of the heart 
known as angina pectoris. 

Angina Simplex. — This is inflammation of the pharynx, with, of 
course, more or less swelling and infiltration of exudate. Swallowing 
may be difficult. Local depletion and sedative washes, with general 
derivation, are indicated. If chronic, stimulant washes are useful 
combined with general tonic treatment. 

1 Dental Cosmos, 1911, p. 296. 

2 For an exhaustive article see Oliver, Dental Cosmos, 1908. 



ANGINA 787 

Ludwig's Angina.— In 1S3G Ludwig described a disease which is 
considered to be an infections cellulitis in the submaxillary region, 
which may extend deeply into the tissues of the neck. The infection 
is thought to be due to the Streptococcus pyogenes or bacillus of 
malignant edema, though the Staphylococci and Diplococcus pneu- 
monia? are found, and probably enter the cellular tissue of the 
submaxillary region and neck through the oral or pharyngeal mucous 
membrane or a wound. An apical abscess, also, the repeated impac- 
tion of food into the peridental region, especially about a third 
molar, and its fermentation has caused a deep infection resulting in 
this disease. The patient has lassitude, chilliness, and fever. 

A hard swelling appears beneath the mandible after several days, 
and extends toward the neck and under the tongue. There is mus- 
cular rigidity and the head is inclined in one direction. The skin is 
not much reddened. 

Later edema is marked and may extend upward toward the 
parotid gland or the glottis. Breathing and swallowing are rendered 
difficult by oral and pharyngeal swellings. There are the usual oral 
symptoms of inflammation. Upon incision the connective tissues 
are found to be sloughing, grayish black in color, and may ooze pus. 

The board-like hardness of the floor of the mouth and the marked 
dyspnea are constant features. 

The spread of the infection being by continuity of cellular spaces, 
the glands are much enlarged. 

A large abscess may form and discharge. Pneumonia, septicemia, 
and pyemia are complications to be feared as the result of spreading 
infection. Incisions for drainage and antisepsis are usually con- 
joined with systemic treatment, but as the case is often of dental 
origin the cause should be removed. 

Vincent's Angina. — This is an edematous tonsillitis, which may 
affect also the mucous membrane of the mouth and pharynx, fol- 
lowed by the formation of a pseudomembrane as in diphtheria, later 
ulceration and hemorrhage may appear. There are the usual accom- 
paniments of inflammation in this locality, together with fever and 
sometimes rigors. It usually lasts about two weeks. It also occurs 
about the gums without necessarily affecting the pharynx, and here 
may last much longer. 

The differential diagnosis from diphtheria and syphilis is made by 
microscopic examination. Vincent's bacilli, spindle-shaped, pointed 
at extremities, and 6 to 10//. in length, are usually associated with a 
long thin spirillum. (See Fig. 611.) 

They take several stains, but not the Gram. In diphtheria, 
Loeffler's bacilli, and in syphilis the treponema pallidum would be 



788 INFECTIONS OF AND FROM THE MOUTH 

found. Tuberculosis, gonorrhea, stomatitis, and pyorrhea must 
also be differentiated. (Lederer.) 

In the treatment mercuric chlorid 1 to 10,000 in 4 per cent, boric 
acid solution, and especially salvarsan, 10 per cent, in sesame oil, 
suspended by the aid of Iodipin (Merck) is recommended for injec- 
tion into the pockets or applied to the gum, are highly recommended 
by Lederer. The writer has cured a number of cases of this type 
by the use of mercuric chlorid, 1 grain in each four ounces of H 2 2 . 
A microscopic examination was not made. 1 Vaughan recommends 
silver nitrate, 4 to 8 per cent., Lugol's solution, chromic acid, 10 per 
cent., zinc chlorid, 2 per cent., and Argyrol full strength, also a light 
diet and cathartics. 

DENTAL STERILIZATION. 

It must ever be borne in mind that the dental operator constantly 
works in a field of infection, and unless extraordinary precautions be 
taken every instrument which touches this field — the fingers of the 
operator, his mirrors, glasses, napkins, rubber dam, rubber dam 
clamps — becomes immediately infected as soon as it is brought in 
contact WTth the mouth of the patient. The likelihood of infection 
varies with the patient and the particular instruments; mouth 
mirrors, rubber dam clamps, scalers, and all instruments used in the 
treatment of pulp canals are likely to become more promptly and 
extensively infected than other instruments. Again, the forms of 
the instruments determine whether or not increased opportunity is 
given for the retention of infective material. The fingers of the 
operator may be the medium through which infective material is 
transferred from one patient to another. Infection may be carried 
from superficial areas of the mucous membrane of the mouth, from 
the enamel and the saliva, into deeper structures, where conditions 
are favorable for the development of sepsis. 

The scheme for dental sterilization, therefore, includes the steriliza- 
tion of the operator, instruments, apparatus, appliances, etc., used 
in. operations, and the sterilization of the field of operation prior to 
operating. 

The Operator. — Extreme personal cleanliness upon the part of an 
operator is clearly the first step in asepsis. The best class of dentists 
are exceedingly neat as regards personal habits; daily bathing, care of 
the nails and of the skin, and immaculate linen form as much a part 
of the day's labor as dental operations per se. The virtues of soap 

1 For an exhaustive article see Vaughan, Dental Cosmos, June, 1912. 



DENTAL STERILIZATION 789 

and water, wherever they may be applied, are regarded as a very 
important item in preventing infection. 

Linen which has been boiled prior to wearing may be regarded as 
safely sterile; so that the matter of personal sterilization relates to the 
hands, particularly to the finger-nails. The space under the nails is 
a favorable habitat for many organisms, notably the pyogenic cocci, 
the staphylococcus pyogenes aureus being commonly present in this 
situation. 

It has always been advised that the finger-nails be trimmed short, 
and be made smooth to avoid mechanical injury to the soft tissues 
of the patient. Since the advent of aseptic and antiseptic surgery 
these precautions have an additional significance; nails kept short 
and smooth may be more readily cleansed than if long and ill-kept. 
The nails should be cut so that they nowiiere project beyond the tips 
of the fingers. Their mechanical cleansing should be done with 
smooth instruments, not sharp knife-blades; the latter produce 
rough surfaces, which furnish spaces for lodgement of bacteria. There 
is but one effective method of washing beneath the nails; it is that 
followed by the general surgeon. After dipping the soap in water as 
hot as can be borne by the hands, all of the finger-nails should be 
made to scrape the soap until the spaces under the nails are filled 
with soap. After this coarse hand-brushes are used to scour every 
part of the hands with soap and water as hot as can be borne. Special 
nail-brushes are next used to scrub beneath the nails, driving out 
piecemeal the soap masses there. The general surgeon continues the 
scrubbing until the nails are scrupulously clean. The soap usually 
used is Castile, or soap made from palm oil, etc., but antiseptic 
soaps, such as ethereal soaps, may T be substituted wdth advantage. 
Tincture of green soap is effective (see below) . 

Sterilization of the cleansed hands is insured by immersing them 
for five minutes in antiseptic solutions, such as 50 per cent, alcohol. 
The hands should be sterilized after treating each patient; rubbing 
the hands with a paste of mustard, flour, and w^ater for three minutes 
and washing off with sterilized w T ater is effective. (Nancrede.) If 
the patient dismissed has possessed an unusually septic mouth, or has 
been a syphilitic, for example, the time for hand cleansing and ster- 
ilization is to be prolonged; if syphilitic, every instrument used is 
transferred to separate vessels containing antiseptic solutions or 
boiled, and the hands are viewed as highly infected; they are scrubbed 
with mercuric chlorid solutions to prevent personal infection or the 
carriage of infection. Chancres have from time to time appeared 
upon the fingers of dentists as w r ell as physicians. In a known 
syphilitic case one might use the rubber gloves worn by surgeons, at 
any rate ,all abrasions should be covered with collodion. 



790 INFECTIONS OF AND FROM THE MOUTH 

Sterilization of Apparatus. — The scrupulous cleanliness of the oper- 
ating chair, of which the head-rest should receive frequent changes of 
boiled linen coverings, the metallic parts should be rubbed, and general 
covering cleansed; the cleansing, polishing, and sterilizing of cuspidors; 
the changing of paper coverings upon instrument tables, etc., are part 
of the general scheme of sterilization. The floor of the operating 
room also requires attention; instead of being covered with carpet, it 
is preferable to have it made of .parquetry material or cement, over 
which rugs are laid, which may be removed from the room for 
cleansing; the floor proper being scrubbed. 

Napkins used about the mouth are certain to become infected, so 
that their boiling should be prolonged at least fifteen minutes. For 
many operations it is preferable to substitute strips of muslin for 
linen napkins, which after being used may be thrown away. 

If a hydraulic saliva ejector be used, the glass mouth tubes should 
be changed for each person, a sterilized tube being substituted 
directly before its use is required. A number of these tubes should 
be in use, and may be sterilized after washing by placing them in a 
50 per cent, solution of listerine or a formaldehyd solution for a few 
hours. Tumblers and mouth mirrors may be sterilized in like 
manner. The cloudiness of saliva tubes is produced by the forma- 
tion of salivary calculus, and may be removed by the use of acidulated 
water. 1 

At the close of each day a large cup should be filled with an anti- 
septic solution, which is to be drawn through the tubing of the ejector 
to keep it in a reasonably aseptic condition. 

Rubber dam may be sterilized by boiling water, but it is more 
safe and cleanly to use a new piece for each patient. It should be 
washed and then dusted with borated talcum powder. 

The water used for douching cavities should be boiled previous to 
placing in the warmer, and should have a little pleasant antiseptic 
added to it. 

Nancrede 2 states that all pyogenic cocci, and even anthrax spores, 
are killed by boiling instruments for two minutes in a 1 per cent, 
solution of sodium carbonate, which also prevents rusting. 

Mouth mirrors and other instruments which can be wet may be 
placed for one-half hour or longer in a covered jar containing 20 per 
cent, formaldehyd, to which borax has been added to saturation. 
Rusting is prevented by borax (Williams). 

Broaches, trephines, and other small points requiring to be kept 
sterile may be placed in a bottle such as are sold containing gold 
cylinders, and kept wet with any essential oil or carbolic acid. 

1 Thornton: Dental Review, 1903. 2 Park's Surgery by American Authors. 



DENTAL STERILIZATION 791 

G. Zederbaum 1 suggests sticking the shanks in the cork; when to 
be used the cork is to be transferred to another bottle of like size 
containing alcohol and shaken to remove the antiseptic. They may 
then be washed in sterilized water. 

Extracting forceps require careful mechanical cleansing and pro- 
longed boiling after each use, for perhaps more cases of infection, 
and of many kinds, have resulted from unclean forceps than from 
all other causes combined. 

Instruments, such as hand-pieces, w T hich cannot be conveniently 
wet may be wiped off with alcohol and then subjected for thirty 
minutes to formaldehyd gas, any closed vessel may have cotton rolls 
saturated with liquid formaldehyd placed therein. Enough gas is 
given off to disinfect. Lacking a special apparatus an aluminum 
omelet pan w T ith the handle filed off makes a convenient and not 
unsightly sterilizer. If desired, all the instruments may be so steril- 
ized. These methods involve the employment of several instruments 
of each kind, an economy of time in any event. The entire instru- 
ment case may be disinfected by placing a formalin tablet in each 
drawer (Miller). 

Sterilizing the Field of Operation. A good method is to forcibly 
spray the mouth with a 1 to 3 per cent, solution of hydrogen dioxid, 
in order to force infective material from about the teeth. The other 
solutions, as a solution of potassium permanganate or mercuric 
cholorid or alcohol may then be used. This spraying or washing 
should be somewhat prolonged when the mucous membrane is likely 
to be injured, as in extractions which often result in infection from 
the patient's own secretions. Many operators keep a stock of inex- 
pensive toothbrushes for such cases, which are thrown away after the 
patient has used them, who is directed to scrub the teeth well with 
the brush and the antiseptic solution. 

For very thorough disinfection thoroughly cleanse the teeth and 
use the antiseptic between them upon floss silk. For surgical w T ork 
or etherization very active work should be done. Wadsworth, 2 in 
an investigation of mouth washes and their action on pneumococci, 
found but little value in the ordinary wash or even solutions of 
formalin, lysol, or H2O2. He found that 

3— Alcohol 30. parts 

Water 70 parts 

Glycerin and salt, a small quantity added. 

was very effective in destroying the bacteria. 

1 Dental Cosmos, 1907. 2 Ibid. 



792 INFECTIONS OF AND FROM THE MOUTH 

In a series of tests upon the devitalizing power of germicides for 
streptococcus, gonococcus, pneumococcus, and Bacillus typhosus, 
Post and Nicoll 1 found tincture of "green soap" (a brownish liquid 
composed chiefly of alcohol and caustic potash), alcohol in solutions 
above 50 per cent., silver nitrate solution from 1 to 1000 to stronger, 
tincture of iodin, Senn's solution (iodin 1, potassium iodid 1, water 
100 and even 400), phenol, 5 per cent., and chloroform were effective 
in one minute. 

Potassium chlorate, mercuric chlorid, 1 to 500, failed in ten minutes. 
Boric acid failed in two hours. As some of these germicides are for 
the mouth and some for the hands the information is of great practical 
value. Perhaps the best method of sterilizing gums for injections 
or gum margins for work is to spray off any accumulation and apply 
tincture of iodin for a few minutes. 

The routine practice of scaling and polishing the teeth and pre- 
scribing an antiseptic mouth wash prior to the commencement of a 
series of sittings is to be highly commended. 

In scaling the writer uses antiseptic washes freely during the 
entire operation. 

If ulcerations or inflammatory conditions exist, the sterilization 
is to be prolonged. If a suspicion of syphilis exist, not only should 
the mouth be freely washed with strong antiseptics, but special 
instruments should be used, preferably an old set, kept sterilized and 
used only in special cases. 

A deep infection may usually be prevented during the treatment 
of pyorrhea alveolaris and pulp gangrene by attention to the ster- 
ilization of the infected tract before beginning work upon the parts 
or during its progress. These methods have been indicated in the 
discussion of these subjects. 

1 Spence: Dental Cosmos, 1911, p. 548. 



INDEX. 



A 



Abnormal food supply, 28 

nerve suppty, 29 

physical conditions, 29 

waste removal, 29 
Abrasion, 300 

acids in, 306 

in animals, 308 

of calculus, 306 

degrees of, 301 

during sleep, 301, 311 

effects of, 307 

from clasp, 306 

gritty powders as cause of, 305 

labial and approximal, 303 

Ungual, 307 

occlusal, 300 

pulp hyperemia in, 477 

relation to caries in, 303, 307 

tooth-brush in, 306 

treatment of, 309 
Abscess, apical, acute, 586 
causes of, 586 
clinical history of, 593 
diagnosis of, 595 
extraction in, 603 
guards in, 599 
pathology of, 588 
scar threatened in, 606 
stages of pus formation in, 

589 
symptoms of, 588 
systematic stopping in, 

613 
systemic complication in, 

604, 607, 630, 643 
treatment of, 598 
varieties of, 592, 597 
chronic, 609 

blind, 631, 642 
necrosis from, 635 
scar from, 534 
symptoms of, 617 
in temporary teeth, 638 
treatment of, 618 
with fistula, 614 
without fistula, 609 

around third molar, 234 

fistula in, 134, 614 

perforation of bone in, 601, 614 

pericemental, 745 



Abscess, pointing in, 134, 604 

of pulp, 497 

pus in, 134 

syringe, 619 
Absence of teeth, 275 
Absorbent organ, 217 
Acacia, use of, 207 
Accidents to teeth, 671 
Acetanilid as cause of hemorrhage, 120 

use of, 400, 491, 605 
Acidity, hvper-, 98, 102, 307, 359, 415, 

740, 741 
Acidosis, acids in, 93 
Aconite, tincture of, 124, 234, 476 
Aconitin, use of, 234 
Actinomycosis of mouth, 780 
Aerogenic bacteria, 45 
Adenoids in mouth breathing, 224, 228 
Adrenalin, use of, 403, 517 
Age as predisposition, 31 
Agenesia of enamel, 260 
Agglutination, 61 
Air warm, use of, 401 
Albumin, fermentation of, 47 
Albuminuria, 112 
Alcohol, injection of, 765 

use of, 150, 401, 423, 789, 791, 
992 
Alexins, 54 

Aloin compound, use of, 689 
Alopecia, from dental disease, 763 
Alteration, definition of, 21 
Alum, use of, 483, 490, 491, 612 
Alveolar process, fracture of, 672 
Alveolitis, postextraction, 603, 633, 672 
Amalgam, copper, use of, 430, 561 

facing, 527 
Amboceptors, 61 
Ameba of dysentery, 38 

properties of, 18 

of pyorrhea, 714 
Ameloblasts, 160 
Ammonia, use of, 423, 642 
Ammonol, use of, 400 
Amputation of roots, 619, 623, 727 
Amyl nitrite, use of, 519 
Anemia, 114, 116 
Anesthesia of apical tissue, 520 

conductive, 407, 482, 520 

diplceic, 408 

general, use of, 398, 515 

mucous, 407, 482 

(793) 



794 



INDEX 



Anesthesia of nerve trunk, 407 

by pressure. See Pressure. 

of pulp, 404, 407, 515 

reflex, 409 
Angina, Ludwig's, 235, 787 

simplex, 786 

Vincent's, 675, 681, 787 
Angle, classification of malocclusion by, 

223 
Ankylosis, dental, 654 
Anomalies of teeth. See Malformations. 
Antikamnia, use of, 400 
Antipyrin, use of, 764 
Antiseptic powders, antiseptic washes 

and, use of, 439, 679, 738, 791 
Antitoxin, formation of, 57 

streptococcus, use of, 150 
Antrum, empyema of, 626 
Aphthae, 769 

Aqua regia, use of, 536, 549 
* Aristol, use of, 429 

Arsenic, accidents with, 528 

action of, on gum tissue, 528 
on pulp tissue, 521 
variations in, 513 

apical hyperemia from, 521 

coverings for, 527 

formulae for, 525 

iodide of, use of, 488 

mummifying paste and, 530 

necrosis from, 529 

objections to, 524 

pocket for, 528 

pulp hyperemia from, 521 

in pulp nodule, 464 

resistance to, 464, 492, 524 

second application of, 524, 528 

suffusion from, 522, 524, 531 

use of, 492, 525 

danger of, 492, 528, 645 
Arsenical fiber, 526 
Asperin, use of, 491 
Astringents, use of, 126, 679, 738 
Atomizer, use of, 739 
Atrophy, 79, 253 

marginal, of gum, 690 

Harlan's method in, 690 
Atropin, use of, 381, 649 
Attachment of teeth, 265, 266 
Auto-intoxication, general malnutrition 
as cause of, 93 

oral, effects of, 684 



B 



Bacteria, action of gastric juice upon, 
54 
aerogenic, 45 
in blood, 44, 49 
as cause of disease, 36 

of inflammation, 131 
chemical composition of, 39 
chromogenic, 45 



Bacteria, classification of, 41 

conditions antagonizing, 53 

of dental caries, 340, 342, 343, 
362, 378, 633 

destruction of, by tissue, 53 

division of, in blood, 45 

effect of blood reaction upon, 64 

external antagonistic agencies, 65 

facultative, 45 

fermenting action of, 45 

ferments of, 46, 47 

forms of, 41 

immunity to, 56, 57, 61 

intoxication and general infection 
by, 44, 48, 49, 53, 55, 136, 146, 
148, 234, 439, 603, 631, 742, 781 

life of, conditions of, 40, 45 

localization of, 44 

media of, 40 

motility of, 40 

of mouth, 50 

obligate, 45 

parasitic, 44 

pathogenic, 49, 51 

penetration of root tubules by, 640 
of secondary dentin by, 457, 
498 

photogenic, 45 

plaques of, 348, 362 

position in vegetable kingdom, 36 

predisposition to, action of, 30, 31, 
50 

products of, 48 

pyogenic, 132 

resistance to, 53 

saprophytic, 45 

spore formation of, 43 

spreading of, in tissue, 49 

zooglea of, 43 

zymogenic, 45 
Bacterial plaques in dental caries, 340, 

362 
Balsam of Peru, use of, 622, 624, 634, 

738 
Band, dental, 159 
Bandage, use of, 126 
Beck's bismuth paste, 622, 624, 625, 739 
Benzoic acid, use of, 679 
Benzoin, use of, 476, 482, 490 
Bilein, use of, 689 

Bismuth, subnitrate, use of, 207, 739 
Black, glands of, 165, 193 
Black's 1-2-3 mixture, use of, 739 

operation for scar, 630 
Blastomycosis, 39, 769 
Bleaching agents, use of, 581 
Blindness, dental, cause of, 762 
Blisters, use of, 125 
Blood, alterations in, 113 

bacteria in, 44-49 

coagulation of, 116 

extravasation of, 119, 126, 480, 484, 
507 

pressure, 123 



INDEX 



795 



Blood, reaction of, as immunizing 

factor, 64 
supply to teeth and jaws, 190 
Bloodletting in inflammation, etc., 138, 

236, 491 
Blue light, us.- of, 400, 599, 642 
Bodkin, wire, use of, 442 
Bone, caries of, 89, 144, 617, 635 
of face, embryology of, 153 
infection of, from dental lesions, 

633, 635 
inflammation of, 142, 633 
of jaw, crypts of, 100 

development of, 165 
necrosis of, 145 

from alveolodcntal abscess, 633 
from syphilis, 595, 780 
perforation of, in abscess, 601, 614 
regeneration of, 146 
. resorption of, 146, 687 

in gingivitis, 690, 701 
septa, 166 
Borax. See Sodium biborate. 
Boric acid, use of, 764 
Boroglycerin, use of, 680 
Brewer's yeast, use of, 137 
Broaches, Downie, use of, 534 
Swiss, 554 
use of, 534, 554 
Bromural, use of, 400 
Brush, use of, 439 
Bruxomania, 301 



Caffein, use of, 605, 764 
Calcareous infiltration, 87 
Calcific degeneration of pulp, 466 
Calcification of teeth, 161 

tubular, 449 
Calcium chloride, use of, 121 
lactate, use of, 121 
salts in blood, 696 
in pus, 711 
Calcoglobulin, 161, 164, 454, 462 
Calcospherites, chemical composition of, 
161 
in dentin, 180 
in enamel, 176 
in pulp nodule, 460 
Calculi, basis of, 88, 693 
Calculus, analysis of, 694 
hematogenic, 711 
origin of, 693 
pyogenic, 711 
salivary, 692 

analysis of, 694 
foreign bodies in, 695 
hardening of, 699 
hematogenic, 711 
mode of deposit of, 698 
occurrence of, 693 
organic factor of, 697 



Calculus, salivary, origin of, 093 

pathological effects of, 701 
pyogenic, 711 
removal of, 704 
scalers for, 702, 703, 704 
structure of, 695 
treatment of, 704 
varieties of, 692 
sanguinary, 711 
subgingival, 708 
Calendula, use of, 680 
Callahan method, 536 
Calomel, use of, 321, 776 
Campho-phenique. See Phenol camphor. 
Canada balsam, use of, 423, 553 
Canals, accidents in opening, 548 
continuity of, lost, 432 
fillings, removal of, 575, 641 
imperfectly filled, results of, 641 
root, enlargement of, 533 
topography of, 541-543 
Cancrum oris, 772 
Cantharides, use of, 532 
Cantilever wire spur, use of, 678 
Capping for pulp, 427 
Capsicum plaster, use of, 476 
Carbohydrates in dental caries, 340, 344, 

347 
Carbolic acid, use of, 207, 235, 401, 411, 
412, 414, 418, 475, 490, 496, 520, 531, 
601, 739, 619 
Carbon dioxid, defective elimination of, 
96, 316 
paper, use of, 666 
Carcinoma, 78, 784 
Caries of bone, 89, 144, 617, 635 
dental, 337 

acids in, 343 

neutralization of, 376, 415, 
443 
age in, 357 
alkalies in, 443 
arrangement of teeth in, 351 
bacteria of, 342, 344, 364, 369, 

378 _ 
bacterial plaque in, 348, 362 
bodily condition in, 358 
calcareous waters in, 357 
causes of, 340, 344, 347 
bacterial, 340, 342, 344 
exciting, 339 

synopsis of, 340 
predisposing, local, 349 
systemic, 356 
in cementum, 384 
chemical reactions in, 344, 376 
clinical history of, 385 
deep-seated, 416, 418 
defects of fillings in, 351, 379 
dentin in, 371 

decalcification of, 372 
secondary, 382, 388 
diagnosis of, 390 
diet in, 346, 352, 361, 445 



796 



INDEX 



Caries, dental, eburnation in, 383 

effect of malnutrition upon, 96 

in enamel, 362, 340 

experiments in, 341 

ferments in, 341, 375, 377, 379 

filth as a protection from, 349, 
361 

foodstuffs in, 346 

glycogenic, 346, 355, 358, 360 

heredity in, 356 

history of, 337 
clinical, 385 

inception of, 340, 362, 385 
location of, 362 

lactates formed in, 343, 376 

lactic acid in, 343 

liquefaction foci in, 378 

loss of crown by, 431 
of root by, 431 
of tissues in, 380 

Miller's general experiments 
on, 341 

morbid anatomy of, 362 

mucin in, 355 

of Nasmyth's membrane, 371 

pathology of, 362 

penetrating, 387 

perforation by, 389, 428 

periodicity in, 357 

pigmentation in, 383 

prenatal influence in, 356 

prognosis of, 392 

progress of, 386 

saliva in, 354, 443 

prophylaxis of, 437 

pulp in, almost exposed, 421 
exposed, 425 

recurrence of, 436 

relative liability of teeth to, 385 

saliva in, 354, 443 

school children and, 357, 358, 
438 

of secondary dentin, 382-388 

self-healed, 371 

simple, 416, 417 

spreading, 387 

stages of, 396 

structure of teeth in, 352, 388 

sulphocyanate in, 359, 360 

superficial, 416 

symptoms of, 390 

of temporary teeth, 432 

terminations of, 388 

therapeutics of, 416 

toxic effects of, 438 

transparent zone in, 380, 387 

tube casts in, 380 

under fillings in, 379 
Caroid, use of, 137 
Caseation, 83 

Castor oil, use of, 207, 634, 764 
Catabolism, 23 

Cataphoresis in hypersensitive dentin, 
403, 419 



j Cataphoresis, use of, 520 

! Cataplasma kaolini, use of, 237, 600, 

605 
j Cathartics, use of, 125, 600 
Caush, tubes of, in enamel, 174 
Caustics, use of, 137 
Cautery, actual, use of, 311, 415 

electric, use of, 311, 415 
Cavitine, use of, 418, 419, 423 
Cells, chemical changes in, 23, 24 

composition of, 17 

giant, 67, 218 

hypertrophy of, 67 

life conditions of, 25 

movements of, 18 

nucleus of, 18 

properties of, 19 
phagocytic, 19 

receptors of, 24, 59 

reproduction of, 20 

stimulation of, effects of, 20, 21, 66 

stimuli of, 20 
Cellulitis, submaxillary, 787 
Cement substance, 162, 163, 167 
solution of, 363, 368 

oxychlorid of zinc. See Zinc. 

oxyphosphate of copper. See Cop- 
per. 

oxysulphate of zinc. See Zinc. 

silicate, use of, 322, 418 

zinc phosphate. See Zinc. 
Cementum in dental caries, 384, 417 

formation of, 167 

histology of, 167, 182 

malformations of, microscopic, 250 

nutritional relation to dentin, 183 

relation of, to enamel, 174, 182 

repair of, 324 
Chalk mixture, use of, 207 

use of, 414, 442 
Chancre of hands, 789 

of mouth, 777 
i Cheek, distention of, by air pressure, 
576, 621 

swelling of, 605 
Chemotaxis, 55 
Chewing gum, use of, 444 
Chloroform, use of, 234, 418, 476, 482, 

551 
Chloro-percha, use of, 398, 414, 476, 

482, 575 
Chlorophyll, chemical action of, 39 
Chlorosis, 115 
Chorea from dental disease, 653 

from dentition, 232 
Chromogenic bacteria, 45 
Cinchona, use of, 738 
Cinnamon, oil of, use of, 739 
Circulation, disturbances of, 113 

local, 122 
Cleansing of teeth, 439, 705 
Cleft palate, embryology of, 156 
Clot, absorption of, 142 

healing under, 142 



INDEX 



797 



Clot, septic, 119, 151 
Cloudy swelling, 83 

Cloves, oil of, use of, 401, 414, 427, 475 
Coagulants, use of, 121, 410, 526 
Coagulation of blood, 116, 130, 132 

necrosis, 90, 132 
Cobalt, use of, 526 
Cocain, systemic effects of, 519 

use of, 403, 411, 475, 515, 634 
Codein, use of, 491 
Cold, use of, 124, 138, 204, 236 
Colloid degeneration, 86, 511 
Coloboma, 81 

Colophony, use of, 414, 553 
Color of teeth, 299, 329, 580 
Complement, 61 
Compress, use of, 120, 126, 606 
Concrescence of teeth, 263 
diagnosis of, 233 
Conical teeth, 253 
Constipation, dental pain from, 763 
Copper amalgam, use of, 430, 438, 507 

oxyphosphate of, use of, 415, 507 

sulphate, use of, 738, 781 
Cords, dental, 159, 170 
Cotton root dressings, 554, 574, 621 

salicylized, use of, 725 

tampons, danger of, 604, 633 
Counterirritants, use of, 145, 476 
Counterpressure in opening tooth, 598 
Crede's ointment, use of, 150 
Creosote, use of, 552 
Cresol, use of. See Formocresol. 
Crowns, cantilever, use of, 430 

loss of, by caries, 431 

removable, 584 

use of, 431 
Crypts of teeth, relations of, 166, 170, 

175 
Cup gum, use of, 621 
Cups, use of, 125 
Curette, use of, 137 
Cusps, supplemental, 270 
Cycle, vicious, 30 

Cysts, associated with apical conditions, 
614, 642 

causes of, 68 

dentigerous, 69, 283 

dermoid, 69 

teeth in, 70 

impacted teeth as cause of, 68, 283 

varieties of, 68 



Deafness, dental, cause of, 653, 762 
Decalcification of dentin in dental caries, 
372 

of teeth, 66, 217 
Degeneration, 81 

calcific, of pulp, 466 

cloudy, of pulp, 511 

colloid, 86 



Degeneration, colloid, of pulp, 511 
fatty, 81 

of pulp, 5 1 1 
fibroid, 507, 669 
of pericementum, 661, 669 
of pulp, 507 
hyalin, 85 

in mouth, 85 

of mucous membrane, 85 
lardaceous, 86 
mucoid, 85 

of mucous membrane, 85 
of nerve-end of pulp, 514 
of pericementum, 661 
Dehydrator, use of, 401 
Dentifrice, use of, 443 
Dentin, caries of, 371 

decalcification in, 371, 422 

secondary, 450 
development of, 161 
granular layer of, 181, 249 
histology of, 176 
hypersensitivity of, 181, 393 

causes of, 393 

diagnosis of, 390, 393 

pathology of, 393 

symptoms of, 396, 753 

treatment of, 398 
interglobular spaces in, 249 
lines in, 176 

of Schreger in, 176, 250 
malformations of, microscopic, 

247 
nutritional relation of, to cementum, 
183 
to dentin, 183 
recalcification of, 424 
repair of, 324, 450 
resistance to acid by, 660 
resorption of, 487, 504 
secondary, 182, 424, 450 

bacterial penetration of, 457, 
498 
staining of, 334, 383 

by putrefaction, 580 
stains of, treatment of, 335, 580 
tubes of, 176 

tubular calcification of, 449 
tumor of, 453 
Dentinal fibrils, 162 

papilla, 159 
Dentition, cause of, 194 

constitutional states modifying, 

200, 214, 231 
normal, 198 
pathological, 198 

as cause of epilepsy, 200 

climate and weather in, 200 

convulsions in, 203 

diet in, 208 

first, 198 

headache in, 203 

hemophilia in, 206 

hemorrhage after, 205 



798 



INDEX 



Dentition, pathological, intestinal com- 
plications in, 201, 
207 
feeding after, 208 
lancing in, 204 
nervous disturbances in, 199, 

202, 213 
paralysis in, 203 
pulmonary disturbances in, 204 
saliva in, 198 

shock after lancing in, 206 
skin disorders in, 204, 206 
strabismus in, 204 
symptoms of, 200, 202 
systemic conditions influenc- 
ing, 200, 214, 231 
treatment of, 204 
periods of, 197 
process of, 196 
second, 215 

disorders of, 230 
irregularities of, 220 
necrosis in, 231 
pathological, 232 
symptoms of, 196, 198 
Depletion of gum, 491 

of pulp, 491 
Derivation, use of, 125, 213, 236 
Dermoid cysts, 69 

teeth in, 70 
Development of face, 153 

of teeth, 159 
Devitalization of pulp, 521 
Devitalizing fiber, use of, 516, 526 
Diabetes mellitus, 101 
Diagnosis, definition of, 26 

forms of, 26 
Diathesis, acquired, 94 
gouty, 104 
hemorrhagic, 119 
hyperacid, 93 
Dilaceration of teeth, 267 
Discoloration of teeth, 329, 580 
Disease, bacterial causes of, 36 
basis of, 25 
causes of, 28 
exciting, 28 
predisposing, 30 
clinical history of, 26 
existing, as a predisposition, 33 
functional, 25 
predisposition to, 30 
previous, as a predisposition, 33 
of teeth, 666 
Dislocation of teeth, 671 
Distomolar, 279 
Dobell's solution, use of, 626 
Donaldson cleaners, use of, 534 
Dover's powders, use of, 600 
Downie broaches, use of, 534 
Drill, Gates-Glidden, use of, 537 

spear, use of, 598 
Dropsical infiltration, 86 
Drugs, intoxication by, 100, 774 



Dry cups, use of, 125, 621 

socket, 634 
Dryness, use of, 401 
Dunn syringe, use of, 738 
Dwarfism of teeth, 251 
Dysentery, ameba of, 38 



Ear, disease of, from dental cause, 653. 

762 
Eburnation in dental caries, 383 
Ecchymosis, 119 

Ehrlich's theory of immunity, 59 
Electrical disinfection of root canal, 612 
Electricity in pulp putrefaction, 577 

as test, 564 
Embalming paste, use of, 551 
Emboli, septic, 119, 151 
Embolism, 118 
Embryology of face, 153 

of teeth, 157 
Emetin, use of, 739 
Emphysema of cheek from air pressure, 

576, 621 
Empyema of antrum, 626 
Enamel, agenesia of, 260 

in dental caries, 340, 362 

development of, 162 

formation of, effect of exanthemata 
upon, 253 

fracture of, 322 

histology of, 172 

hypoplasia of, 253 

imbrications of, 245 

lines of Schreger in, 174 

malformation of, macroscopic, 251 
microscopic, 239 

nodule, 268 

opaque spots in, 240 

organ, development of, 159 

organic matter in, 172, 242 

parts of, 172 

relation of, to cementum, 174 

resorption of, 312 

rod, 163 

sensitivity of, 396 

stains upon, 331 

stria? of, 163, 244 

stripes of Retzius in, 174, 244 
of Schreger in, 174, 245 

tubes of, 173 

Caush's, 173 

unusual location of, 268 
Encystment of teeth, 283 
Endarteritis obliterans, 77, 688 
Energy, nerve, loss of, 110 

sources of, 23, 99 
Epilepsy from dental disease, 200, 653 

pathological dentition as cause of, 
200 
Epizootic stomatitis, 712 
Equinia, 772 



INDEX 



799 



Ergot, use of, 121, 124 
Erosion of teeth, 313 

acids in, 314 . 

extraneous, 317 
effects of, 319 

malnutrition upon, 90, 316 
possible action of glycogen in, ! 

84 
treatment of, 321 
Eruption of teeth, causes of. See Den- 
tition. 
Escharotics, effects of, 29, 645 
Ether, use of, 398, 402, 519 
Ethyl chlorid, use of, 402 
Etiology, definition of, 26, 28 
Eucalyptol, use of, 551, 575 
Euca-percha, use of, 551, 639 
Eugenol, use of, 423, 475, 476 
Evans' root drier, use of, 531, 553 
Exanthemata, 152 

malformations caused by, 152, 253 
necrosis caused by, 152, 214, 231 
Excess of teeth, 278 
Exostosis of alveolar process, 653 
Extirpation of pulp, 532 
Extravasation of blood. See Blood. 
Eye disease of, from dental cause, 653, 
756, 758 



Face, development of, 153 

embryology of, 153 

fistula on, treatment of, 606, 630 
Farradism as test, 564 
Fat, degeneration of, 81 

infiltration of, 81 

necrosis of, 91 
Fermentation, bacteria as causes of, 45 

definition of, 45 

products of, 46 

of proteid matter, 47 
Ferments, organized, 46 

unorganized, 46 

varieties of, 47 
Fever, 146 

Fevers, eruption, 773 
Fibrin, formation of, 116 
Fibroma, 74 

Fibrosis. See Degeneration. 
Filling material, use of, 309, 321, 416, 

426, 438 
Fillings, combination of, 422 
Fistulae, 134 

in antrum, 626 

causes of, 617 

on face, threatened, 606, 630 
treatment of, 630 

healing of, 622 

making artificial, 601, 614 

non-healing of, 621 

packing, 623 

premature closure of, 137, 604 
Flagg's operation for scar, 628 



Fletcher's carbolized resin, use of, 414, 

129 
Flexion of teeth, 267 
Floss silk, use of, 391, 441 
Follicle, dental, 167, 170 
wall of, 161, 168 

becomes pericementum, 168 
Food, chemical changes in, 24 
concentrated, use of, 150 
supply, abnormal, 28, 94 
Formaldehyd, action of, upon products 
of putrefaction, 572 
uses of, 413, 477, 496, 501, 517, 544, 
546, 680, 790 
Formocresol, use of, 496, 546, 612, 639, 

640 
Formo-percha, use of, 551, 578, 612, 621 
Fracture of alveolar process, 671 
of teeth, 322, 571 

repair of, 324, 451 
reunited, 324 
treatment of, 326 
Fungi, animal, 36 
as ferments, 45 
vegetable, 36 
Fungous gum, 429 
Fusion of teeth, 261 



Gall-stones, origin of, 81, 693 
Galvanism, sterilization by, 612 

as test, 564 
Gangrene, 89, 91 

circumscribed, 92 
dry, 91 
moist, 91 

discoloration from, 580 
of pulp, 562 
dry, 562 
moist, 565 
partial, 570, 580 
Gastric juice, action of, on bacteria, 49 
Gaultheria, oil of, use of, 739 
Gelatin, use and danger of, 120 
Gemination of teeth, 266 
Geranium-formol, use of, 572 
Germicides, action of, 65, 791 
Giantism of teeth, 251 
Gingivitis, 673 

antiseptic washes in, 679 
astringent washes in, 679 
deeply seated, 682 

interstitial, 682 
marginal, 674 

resorption of bone in, 687, 701 
systemic causes of, 683 
Glanders, 772 
Glands, pericemental, 165 
Glycerin, use of, 237, 402 
Glycogen in caries, 346, 355, 358, 359. 
360 
infiltration of, 84, 355 



800 



INDEX 



Glycogenic infiltration in dental caries, 

355 
Gonorrhea of mouth, 781 
Gout, 103 

chronic, 103 

contrasted with rheumatism, 108 

diet in, 105 

oral effects of, 747 

relation of, to teeth, 710 

salts deposited in, 103 

treatment of, 105 
Goutiness, 104 

treatment of, 105 
Granulations in regeneration, 138, 146 
Greenfield's artificial root, 625 
Grippe. See La Grippe. 
Guards, use of, 477, 599 
Guillotine, gum, 235 
Gum, depletion of, 491, 604 

glycogenic infiltration of, 84 

hyperplastic, 389, 429, 506 

laceration of, 671 

lancing of, 204, 235, 604 

marginal atrophy of, 690 

Harlan's method in, 690 

tissue, action of arsenic on, 528 
Gutta-percha, eucalvptol solution of, 
use of, 551, 639 

use of, 418, 421, 423, 430, 433, 476, 
507, 550, 638 



Hair, teeth and, 70, 276 
Halisteresis ossium, 146, 687 
Hamamelis distillate, use of, 604 
Hands, sterilization of, 790 
Hare-lip, 157 

Harlan's method in atrophy, 690 
Headache in dentition, 203 

from impaction, 294 

from pulp diseases, 756 
Healing by second intention, 140 

under a clot or scab, 142 
Heat, use of, 137, 606 
Hematogenic calculus, 711 
Hemoglobin, derivatives of, 89, 580 
Hemophilia, 119 

in dentition, 206 
Hemorrhage, acetanilid as cause of, 120 

after extraction, 672 
pulp removal, 518 

replantation for, 121 

treatment of, 120 

varieties of, 119 
Hemorrhagic diathesis, 119 

sex in, 120 
Heredity as a predisposition, 33 
Herpes labialis, 783 

zoster, 783 
Hertwig root, sheath of, 165 
Heteroplasty following amputation of 
natural roots, 728 



High-frequency current, 563, 623, 739 
Histology, morbid, 25 
Hoffendahl, electric method of, 577 
Hot water, use of, 410 
Howship's lacunae, 146, 658 
Hutchinson's teeth, 254 
Hydrastis, use of, 121 
Hydrogen dioxid, 208, 235, 496, 582, 
623, 706, 770 
dangers of, 614 
Hydronaphthol, use of, 623, 691 
Hygiene, definition of, 27 
Hyoscyamin, use of, 400 
Hyperacidity. See Acidity. 
Hyperacidosis, 93 
Hypercementosis, 650 

reflex neuroses from, 653 
Hyperemia, arterial, 122 
collateral, 123 
compensatory, 123 
degrees of, 124 
pathology of, 125 
of pulp, 468 

arterial, 468 

devitalization in, 478 

from arsenic, 521 

from electric action, 479 

from hypercementosis, 653 

idiopathic, 471, 478 

thermal toleration in, 474, 478 

venous, 479 

devitalization in, 524 
from hanging, 482 
reflex, 123 
as a resistance to infection, 124 
results of, 123 
symptoms of, 124, 471, 482 
treatment of, 124 
venous, 125 

suffusion from, 480 
Hypernutrition, 66 
Hyperplasia, 68, 503, 506 
of gum, 389 
of pulp, 389 
Hypersensitivity of dentin, 393. See 

Dentin. 
Hypertrophy of cells, 67 
Hypnotism, use of, 400 
Hyponutrition, 79 
Hypophosphites, use of, 488 
Hypoplasia, 79, 253 
of enamel, 253 
Hysteria, 233 



Ichthyol, use of, 773 
Immunity, 34, 56 

acquired, 57 

blood reaction in, 64 

Ehrlich's theory of, 59 

lost, 35, 56 

natural, 56 
Impaction of teeth, 283 



INDEX 



SOI 



Impaction of tooth, as cause of cysts, 
69, 294 
death of pulp from, 293 
diagnosis of, 295 
headache from, 294 
neuralgia from, 292 
resorption of roots from, 285, 

295, 657 
symptoms of, 292 
treatment of, 296 
Implantation, 625 
Inanition, 99 
Indican as an index for malnutrition, 

100, 685 
Indol, 100 

Infants, feeding of, 208 
Infarction, 119 

of pulp, 507 
Infection, classes of, 49 
general septic, 149 
of mouth, 766 

predisposition to, 30, 31, 56 
resistance of tissue to, 52 
spreading of, 48 
Infiltration, calcareous, 87 
dropsical, 86 
fatty, 81 

glycogenic, 74, 355 
pigmentary, 88 
Inflammation, 127 

bacteria in, 127, 131 
bloodletting in, 138 
of bone, 143 
catarrhal, 130 
causes of, 127 
coagulation in, 129, 132 
derivation in, 138 
exudates of, 126 
infective, 131 
necrosis in, 132 
pathology of, 127, 131 
of pulp, 483 

chronic, 501 
resolution in, 132 
simple, 127 
stimulation in, 138 
suppurative, 132 
symptoms of, 131, 135 

general, 131, 135, 136 
treatment of, 137 
Injury of teeth, 322 
Inoculation by bacteria, 49 
Insanity from dental disease, 294, 759 
Insomnia from dental disease, 439, 762 
Instruments, sterilization of, 790 
Insulator, 311 

Intermaxillary bone, failure of develop- 
ment of, 168 
formation of, 153 
Intestinal complications in pathological 
« dentition, 201, 297 
Intoxications, 100 
acid, 102 

bacteria], 101, 148 
51 



[ntoxicat ions, drug, LOO 

intestinal, 9 \, 68 i 

intrinsic, L01, 102 

sept Lc, 1 18 
Intubation of root, 584 
Involucrum, 145 
Iodin, dental, tincture of, 476 

use of, 235, 412, 476, 507, 530, 549, 
572, 579, 770, 792 
Iodoform, use of, 549, 623 
Iodoglycerol, use of, 738 
Iron, chloride of, tincture of, use of, 
353, 605 

dialyzed, use of, 530 
Ischemia, 122 



Jaw, development of, 153 

growth of, cause of, 172 
Jodoformagen, use of, 423, 427 
Joining of teeth, 421, 699 
Jugulation of pulp, 481 



Kalium natrium, use of, 536, 577 
Karyokinesis, 20 
Kerr broaches, uses of, 534 
Kowarska's paste, 729 
Krameria, use of, 680 



Laceration of soft tissues, 672 

Lactic acid, use of, 738 

Lacunae, Howship's, 146 

La grippe, as cause of reflex pain, 763 

Lanolin, use of, 149, 776 

Laudanum, use of, 121, 672 

Lead, oral effects of, 649 

water, use of, 121 
Leeches, use of, 600 
Leprosy, 786 
Leukemia, 115 
Leukocytosis, 115 
Leukoplakia buccalis, 783 
Lichen planus, 784 
Light, electric, use of, 391 
Lime-water, use of, 446 
Linings, use of, 419 
Listerine, use of, 207, 770, 790 
Lithemia, 106 

Lithia salts, use of, 689, 741 
Liver, functions of, 98 

in general malnutrition, 95, 93 
Ludwig's angina, 235, 787 
Lupus of mouth, 780 
Luxation of teeth, 639 
Lymphangitis, 605 



802 



INDEX 



M 



Magnesia, milk of, use of, 321, 415 

sulphate of, use of, 125, 600, 697 
Malaria, dental pain from, 763 
Malformations, macroscopic, 251 

microscopic, 239 

of roots, 271, 545 

of teeth, 239 
Malnutrition, causes of, 23, 93 

from gingivitis, 742 

general, 93. See Bacteria intoxi- 
cations, 
auto-intoxication in, 93 
diet in, 97, 105 
Malocclusion of teeth, 664 

causes of, 219 

classification of, 223 
Malpositions of teeth, 281 
Massage, use of, 605, 738 

vibratory, 605 
Maxillae, embryology of, 154 
Maxillary rampart, 159 
Mechanical injury of teeth, 322 

union of teeth, 266 
Meckel's cartilage, 158 
Melancholia from dental disease, 762 
Menthol, use of, 401, 482, 496, 540, 764 
Menthol-phenol, use of, 475, 648 
Mercury, bichlorid of, use of, 150, 235, 
559, 605, 621, 624, 648, 649, 681, 
789, 792 

as cause of stomatitis, 648 

oral effects of, 232, 648, 681 

Talbot's experiments on dogs with, 
644 
Metabolism, diseases of, 24, 93 
Metastasis, 56, 144 
Methyl chlorid, use of, 402 
Microorganisms, as disease causes, 36 
Milk, modified, 208 
Mitosis, 20 

Morphin, use of, 138, 399, 491, 600 
Motor reflexes from dental disease, 761 
Mouth, actinomycosis of, 780 

asepsis of, 788 

bacteria of, 50 

pathogenic, 51 

breathing, 224 

development of, 153 

gangrene of, 772 

gonorrhea of, 781 

hyaline degeneration in, 85 

infections of, 766 

inflammation of. See Stomatitis. 

lamp, electric, use of, 390, 626 

sepsis from. See Bacteria intoxi- 
cation. 

soft tissues of, laceration of, 672 

sterilization of, 788 

syphilis of, 775 

tuberculosis of, 780 

washes, application of, 679, 788 
Mucin, characteristics of, 85 



Mucin in dental caries, 355 
Mucoid degeneration, 85 

of mucous membrane, 85 
Mucous membrane, glycogen in, 84 
hyaline degeneration of, 85 
mucoid degeneration of, 85 
overstimulation of, effects of, 
84 
Mummification of pulp, 556, 558 
Mummifying paste, arsenic and, 530 
Mustard, use of, 125, 789 
Myers' syringe, use of, 406, 518 
Myrrh, tincture of, use of, 649, 681 



N 



Nasmyth's membrane, 165, 172 

in dental caries, 371 
Necrobiosis, 89 
Necrosis, 89 

after extraction, 634 

of alveolar bone, 608 

of bone, 145 

arsenical, 529 

from alveolodental abscess, 635 

from syphilis, 636, 775 

coagulation, 90, 132 

etiology of, 89 

of fat, 91 

from exanthemata, 231 

from mercury, 232, 648 

from typhoid fever, 221 

liquefaction in, 91 

phosphorus and, 785 

varieties of, 89 
Neoplasm of pulp, 511 
Nerve energy, loss of, 110 

fifth, 754 

sensory, of face, 754 

supply, abnormal, 29 

trophic influence of, 29 

vasomotor, 122, 29 
Nervocidin, use of, 520 
Nervous disturbances in dental disease, 
203, 752 
in dentition, 193, 204 
Neuman, sheath of, 162, 176 
Neuralgia, cause of, 270, 389 

from hypercementosis, 653 

from hypersensitive dentin, 753 

from impacted teeth, 277 

from pericemental disease, 757 

from pulp disease, 755 

from secondary dentin, 433 

treatment of, 764 
Neurasthenia, 110 
Neuroma, 155 
Neuroses, reflex, 752 
Nitric acid, use of, 311 
Nitrous oxid gas, use of, 398, 491 
Nodule, cemental, 273 

in pulp, 458 
Noma, 235, 772 



INDEX 



803 



Non-conductors, uses of, U9 
Novocain, use of, -107, 518 
Number of teeth, variations in, 275 

Nutrition, basis of, 22 
deficiency of, 79 

disturbances of, 24, 28, 30, 66, 93 
excess of, 66 



Obligate bacteria, 4.5 
Odontalgia, phantom, 759 
Odontoblasts, 160, 178 

atrophy of, 453, 510 

relation of, to sensory nerves, 181 
Odontomata, 273 
Oligocythemia, 107 
Opium, use of, 121, 125. 207, 234, 602 
Opsonic index, raising of, 622, 740 
Opsonins, 62 
Organic matter, decomposition of, 45, 47 

fermentation of, 45 
Organs, composition of, 22 
Orthoform, use of, 413, 429 
Osteitis, condensing, 144 

rarefying, 144 
Osteodentin, 456 
Osteomalacia,. 146, 446, 687 
Osteomyelitis, 143 
Osteoporosis, 144 
Osteosclerosis, 144 
Overarch bar, use of, 664 
Overfeeding, 99 
Overuse of teeth, 661, 664 
Oxaluria, 110 
Oxidation, deficiency of, 93 

excessive, 93 
Oxygen, nascent, use of, 582 



Paix, dental, from other sources than 
dental', 763 

postextraction, 603, 633, 672 
Palate, cleft, cause of, 156 
Papain, use of, 560 
Papoid, use of, 137 
Paraffin, use of, 552, 739 
Paraform, use of, 612 
Paraglossus, 311 
Paralysis from dental disease, 760 

in dentition, 203 
Paramolar, 279 
Parasitic bacteria, 44 
Pathogenesis, definition of, 26 
Pathogenic bacteria, 44, 49 
Pathology, basis of, 17, 25 

dental, definition of, 17 

general, definition of, 17 
Pediluvium, hot, use of, 118, 600 
Peptones, 47, 126 
Perforation by accident, 548 

by caries^ 389, 428 



Perforation as cause of abscess of root, 
619 

rilling of, 561 

in >cp! ic cases, 637 
Pericemental abscess, 7 15 
Pericementitis, 585. Set also Pyorrhea 
alveolaris. 

acute, septic, apical, 581 
extraction in, 602 

beginning at mini margin, t'»7 1 

chronic, sepl ic, apical, 609 

classification of. 585 

gouty, 710 

non-purulent, 639 

non-septic, 644 
chemical, 645 
results of, 650 
symptomatic, 648 

phagedenic, 676 

septic at bifurcations of roots, 643 

symptomatology of, 585 

traumatic, 644 
Pericementum, blood supply to, 190 

calcospherites in, 193 

cellular element of, 186, 193 

degeneration of, 661 
fibroid, 669 

development of, 168 

diseases of, 586 

fibrosis of, 669 - 

function of, 184 

glands of, 165, 193 

histology of, 184 

nerves of, 190 

overuse of, 661 
Periostitis, 143 

maxillary, 617 

proliferative, 143 

suppurative, 143 
Peru, balsam of. See Balsam. 
Petechia, 119 

Phagocytosis, 19, 55, 152, 622 
Phantom odontalgia, 759 
Phenacetin, use of, 400, 491 
Phenobromate, use of, 400 
Phenol camphor, use of, 414, 475, 540, 
672, 689, 739, 771 

sodique, use of, 444, 672, 724, 770 
Phenolsulphonic acid, 619 
Phosphaturia, 111 
Phosphor necrosis, 785 
Phosphorus, use of, 81, 785 
Physical condition, abnormal, 29 
Physiology, morbid, 25 
Pigmentary infiltration, 88 
Pigmentation in dental caries, 383 
Pigments in tissue, 88 
Pilocarpin, oral effects of, 648 
Pins, removal of, 576 
Piscidia erythrina, use of, 400 
Plantation, mode of attachment in, 659 

resorption after, 656 
Plaques, microbic, 348, 362 
Plaster of Paris, use of, 427 



804 



INDEX 



Plethora, 113 
Podophvllin, use of, 689 
Pointing, 134 
Polycythemia, 113 
Porte-polisher, use of, 442 
Potassium bromid, use of, 402 
carbonate, use of, 402 
chlorate, use of, 206, 444, 649, 681, 

792 
hydrate, use of , 411 
permanganate, use of, 
sulphocyanate, use of, 415 
Poultices, danger of, 606 

uses of, 606 
Powder, tooth, use of, 443 
Precipitins, 62 
Predisposition to disease, 30 
general, 30 
local, 33 
Pregnancy, dental pain from, 763 
Pressure anesthesia, 458, 465, 474, 482, 
496, 516 
hemorrhage after, 517 
Process, alveolar, fracture of, 672 
Prognosis, definition of, 26 
Prophylaxis, 26, 437, 445 
Proteid, composition of, 18 
fermentation of, 47 
use of, 23 
Protoplasm, composition of, 18 

properties of, 22 
Protozoa as disease causes, 36 
Pseudoodontalgia, 759, 764 
Ptomains, 44, 47 
Pulp, abscess of, 497 

action of arsenic on, 521 
anesthesia of, 405, 415 
blood supply of, 178 
capping of, 426 
cavity, duplication of, 267 

forms of, 186 
constructive diseases of, 449 
death of, from impaction, 294 

symptoms of, 563 
degeneration of, 507 
calcific, 465 
cloudy, 486 
colloid, 514 
fatty, 511 
fibroid, 507 
nerve, 514 
depletion of, 482, 490 
destructive diseases of, 468 
devitalization of, 521 
digestion of, 560 
exposure of, symptoms of, 425 

treatment of, 422, 426 
extirpation of, 532 
gangrene of, 562 
partial, 570 
histology of, 176 
hyperemia of, 468 
arterial, 468 

devitalization in, 476 



Pulp, hyperemia of, arterial, from 
electric action, 479 
idiopathic, 471, 478 
thermal toleration in, 478 
from arsenic, 521 
venous, 479 

suffusion in, 480 
hyperplasia of, 389, 503 
infarction of, 507 
inflammation of, 483. See Pulpitis. 

chronic, 501 
jugulation of, 481 
knocking out, 531 
mummification of, 556, 558 
neoplasm of, 511 
nerves of, 181 
nodules, 458 

arsenic and, 465 
puncturing of, 482, 490, 531 
putrefaction of, 565 
reaction of, 447 
removal of, 515 
partial, 557 

special methods of, 531 
replantation of, vitality after, 456 
sclerosis of, 501 
sedation of, 475 
suppuration of, 492 
swelling of, 486 
thermal tolerance of, 424 
toughening of, 538 
ulceration of, 493 
vitality of, tests for, 563 
Pulpitis, 483 
acute, 484 
chronic, 501 

from pyorrhea, 666 
hyperplastic, 503 
resorption of dentin in, 487 
Pumice, use of, 705 
Purpura hemorrhagica, 786 
Pus formation, stages of, in apical 
abscess,589 
varieties of, 135 
Putrefaction, 47, 565 
formalin in, 572 
germs of, effects of electricity upon, 

577 
of pulp, 565 
Pyemia, 151, 782 
Pyocyaneo-protein, use of, 637 
Pyogenic calculus, 711 
Pyorrhea alveolaris, 713 

abscess secondary to, 721, 745 
beginning with a marginal gin- 
givitis, 716 
in bifurcations of roots, 727 
breath in, 720 

bridge and plates in, 662, 736 
causes of, 713 
clinical history of, 716 
dental caries and, 687 
diagnosis of, 716, 723 
endarteritis in, 719 



INDEX 



805 



729 



Pyorrhea alveolaris, gum incision in, 726 
recession in, 710 
heteroplasty .of roots in, 728 
interstitial gingivitis in, 683, 

719 
living pulps and, 727 
looseness in, 719 
malnutritions^ factor in, 740 
not dependent upon calculus, 

743 
opsonic index in, 740 
oral catarrh in, 720 
pathology of, 716 
prevention of motion in, 
prophylaxis in, 737, 741 
recurrence of, 741 
replantation in, 740 
root amputation in, 727 
shifting of teeth in, 665, 720 
splints for use in, 729 
systemic effects of, 742 
symptoms of, 716 
treatment of, 724 

medicinal in, 737 
varieties of, 715 
Pyrozone, use of, 531, 582, 624 



Q 



Quinin, use of, 150, 400, 491, 600, 605, 
764 



R 



Rachitis, 110 
Rampart, maxillary, 159 
Recalcification of dentin, 423 
Receptors of cells, 24, 59 
Reflex-action, 199, 201, 203, 761 

disorders of dental origin, 752 
of systemic origin, 763 

neuroses, 752 

pain, 464, 470, 471 
pathology of, 752 
Regeneration of tissue, 138, 146 
Repair of dentin and cementum, 324, 

455 
Replantation, 624 

for hemorrhage, 121 

of pulp, vitality after, 456 

secondary dentin after, 456 

of teeth, 647 
Resorcin, use of, 143 
Resorption of bone, 146 

varieties of, 146, 687 

of enamel, 312 

of permanent roots, 655 

of pulp, 487, 504 

of temporary roots, 216 

perforation by, 219 
Retention of teeth, 221 
Retzius, stripes of, in enamel, 174, 244 



Ethein, root methods of, 53!), 510 
Rheumatism, 107 

chronic, 109 

contrasted with gout, 108 

muscular, 109 

treatment of, 108 
Ridge, dental, 159 
Robinson's remedy, use of, 311, 411, 

415, 418 
Root, ampul a tion of, 619, 623, 727 

artificial, 625 

bifurcation, formation of, 168 

calcification of, 167, 171, 176 

canal, accidents in opening, 548 
anatomy of, 541, 543 
cementum forming end of, 168 
electrical disinfection of, 577 
filling of, 550, 613 
inaccessible foramina of, 544 
loss of continuity of, 432 

development of, 167, 220 

drier, Evans', use of, 531, 552 

filling, immediate, 539, 576 
removal of, 549 

fracture from putrefaction, 571 

fusion and concrescence, 272 

implantation of, 625 

long and short, 270 

loss of, by caries, 389, 432 

malformations of, 271, 545 

multiple, 271 

perforation, 329 

permanent, formation of, 220 
resorption of, 295, 655 

repair of, 324 

replantation of, 647 

resorption of, 216, 219 
of permanent, 655 

soap in, use of, 619, 789, 792 

sterilization of, 571 

systematic stopping, 613 

temporary, resorption of, 216 

transplantation of, 431, 625 
Rose geranium, oil of, use of, 572 
Rubber band, use of, 441 

cup, use of, 621, 705 

sore mouth and, 771 



Saccharin, use of, 207 

Salicylic acid, use of, 679 

Saliva, analysis of, 695 

in dental caries, 354, 443 
in general malnutrition, 93, 314 
increased flow of, 198 
infective bacteria in, 50, 781 
lack of, 354 
m relation of acid food to, 355 

Salivary calculus, 692. See Calculus. 

Salol, use of, 150, 207, 553, 605 

Salter, lines of, in dentin, 176 

Salvarsan, use of, 780 



806 



INDEX 



Sandarac, use of, 429 

Sanguinary calculus, 711 

Sapremia, 148 

Saprophytic bacteria, 4.5 

Sarcoma, 74 

Scab, healing under, 142 

Schizomycetes, 36, 41 

Schreger, stripes of, in dentin, 176 

in enamel, 174, 245 
Sclerosis of pulp, 501 
Scorbutus, 109, 215, 649, 786 

infantile, 215 

oral effects of, 649, 786 
Scurvy. See Scorbutus. 
Sedation, results of, 21 
Sedatives, use of, 475, 482, 490, 501, 648 
Sepsis dental, bacterial intoxication and, 
439 

general, of dental origin, 439, 631, 
781 

intoxication from, bacterial intoxi- 
cation and, 148, 439 
Septicemia, 149, 235, 782 

from apical abscess, 604, 631 
Sequestrum, 89, 92, 145, 785 
Serres, glands of, 193 
Serum therapy, 59, 122 
Sex as predisposing cause of disease, 31 
Sheaths of Neuman, 162, 176 
Side chain theory, Ehr rich's, 24, 59 
Silicate cements, use of, 322, 418, 424 
Silver, Crede's ointment, use of, 150 
soluble, use of, 150 

nitrate, use of, 311, 412, 415, 433, 
438, 477, 530, 624, 770 
Sinus, 134 

Size of teeth, variations in, 251 
Skin eruptions, 152, 204, 632 
Slough, 92 

Soap, use of, 619, 789, 792 
Sodium biborate, use of, 679, 790 

bicarbonate, use of, 412, 423, 490, 
689, 764, 785 

bromid, use of, 213 

carbonate, use of, 411 

chlorid, use of, 412, 549, 681, 689, 
738 

dioxid, danger of, 577 

use of, 336, 412, 549, 576, 582, 
790 

hydrate, use of, 411 

potassium and, alloy of, use of, 536, 
577 

sulphate, use of, 121 
Somnaform, use of, 399, 515 
Sphacelus, 87 
Sponge, use of, 637 
Stains, black, 333 

in dentin, 334 

dyes and, 333 

green, 331 

metallic, 329 

non-metallic, 331 

red, 333 



Stains, tobacco, 333 

treatment of, 334 
Starvation of tissue, 99 
Stellate, reticulum, 160, 164 
Steresol, use of, 297 
Sterilization, dental, 788 
Stimulation, effects of, 21. 66 
Staples, use of, 328, 421, 64:; 
Stomatitis, 766 

aphthous, 769, 772 

classification of varieties of, 767 

in dentition, 204, 206 

epizootic, 772 

follicular, 771 

from drugs, 774 

from eruptive fevers, 773 

from glanders, 772 

infective catarrhal, 767 

mercurial, 768 

beneficial effects of mercury in, 
649, 681 

simple catarrhal, 767 

symptomatic catarrhal, 768 

typhoid, 768 

ulcerosa, 677 

ulcerative, 769 
i Stopping, systematic, 613 
i Strabismus in dentition, 204 
i Stratum intermedium, 160, 165 
: Strontium lactate, use of, 121 
! Structure of teeth, 239, 352, 388 
j Stiychnin, use of, 519, 765 
Subgingival calculus, 708 
Suffusion, 119, 580 

from arsenic, 524, 531 

from hanging, 482 

from venous hyperemia, 480 
Sugar in diabetes, 101, 360, 358 

as source of energy, 24, 99 
Sulphocvanate, use of, 360, 415 
Sulphuric acid, use of, 531, 549, 622, 

624, 738 
Sulphurous acid, use of, 583 
Supernumerary teeth, 280 
Supplemental cusps, 270 
Suppuration in inflammation, 132 

of pulp, 492 
Suprarenal extract, use of, 121 
Susceptibility to disease, 30 
Symbiosis, 49 
Symptoms, definition of, 25 

objective, 26 

subjective, 26 
Synostosis, dental, 654 
Syphilis, dental pain from. 763 

hereditary, 257 

of mouth, 7 ( 5 

necrosis of bone from. 636, 
775 

oral effects of, 254 

stigmata of, 257 
Syphilitic teeth, 254 
Systematic stopping of troublesome 
root, 613 



INDEX 



807 



Tannin, use of, 206, 402 
Tartasol, use of, - 38 
Temperament, classes of. 32 
Therapeutic-, basis of, 21 

definition of, 17. 26 
Thrombosis, 117, 481, 521 
Thymol, use of, 420. 123, 427, 475, 483, 

490, 490, 540 
Thymophen, use of, 475 
Tic douloureux, 404 
Tissue, composition of, 23 

excessive destruction of, 99 

food supply to, 22 

regeneration of, 138 

resistance of, to bacteria, 53 

starvation of, 99 

waste, excessive, 99 
Tomes, granular layer of, 249 
Toxalbumins, 44, 48 
Toxemia. 44, 48, 135, 136, 148 

in general malnutrition, 93 
Toxins, 44, 48 

chemotactic properties of, 55 

as ferments. 44 

immunity to, 57 
Toxoid, 60 
Toxon, 61 
Transparencv of dental structures, 382, 

449 
Transparent zone, 380, 387 
Transplantation, use of, 431, 625 
Trephine, use of, 328, 643, 602 
Treponema pallidum, 256 
Trichloracetic acid, use of, 507, 738, 770 
Trigemin, use of, 492, 600 
Trioxymethylene, use of, 413 
Trophic disturbance, 29 

from dental disease, 763 
Tube casts in dental caries, 380 
Tuberculosis of mouth, 780 
Tubes of dentin, 176 

of enamel, 174 
Tubular calcification, 449 
Tumors, 72 
Turkish baths, use of, 689, 741 



U 



Ulceration, 92, 136 

of pulp, 493 
Uremia, 101 



Urates in pericemenl um, 7 17 

in tissue, 97 
Uric acid in goul . L03 

Uterine disease, dental pain from, 763 
l' vula, bifid, 158 



Vaccixi: therapy, 62, 63, 150 

Yapocain, use of, 402 

Varnish, use of, 419, 421, 423, 476, 477 

Vascular system, disturbances of, 113 

Vaselin, use of, 739, 764 

Vasomotor nerves, 122 

Vegetable fungi, 36 

Venous hyperemia, suffusion from, 455 

Veratrin, use of, 225 

Vibrator, use of, 605 

Vincent's angina, 675, 681 



W 



Wall, follicular, 161 

Waste, removal, abnormal, 28, 94 

Water, boiling, as germicide, 790 

drinking of, 689, 741 

warm, use of, 418 



X-rays, use of, 612, 623, 739 



Ziehler-Hoffexdal, electric method 

of, 612 
Zinc chlorid, use of, 410, 484, 517, 621, 
679, 738 
iodide, use of, 738 
oxid and eugenol, use of, 423, 427, 
476, 489, 638 
use of, 427 
oxychlorid of, use of, 411, 415, 423, 

427, 551, 637 
oxvphosphate, use of, 232, 419 

421, 423, 476 
oxysulphate, use of, 427 
sulphate, use of, 427 
sulphocarbolate, use of, 738 
Zooglea of bacteria, 43 



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